Veterinary World, EISSN: 2231-0916
Available at www.veterinaryworld.org/Vol.15/July-2022/22.pdf
RESEARCH ARTICLE
Open Access
Cellular immune response of Staphylococcus aureus enterotoxin B in
Balb/c mice through intranasal infection
Hidayatun Nisa Purwanasari1
, Amanda Tri Utami Permatasari1 , Fajar Budi Lestari2,3
and Siti Isrina Oktavia Salasia1
Khusnan Zaini4
, Madarina Wasissa1
,
1. Department of Clinical Pathology, Faculty of Veterinary Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia;
2. Department of Bioresources Technology and Veterinary, Vocational College, Universitas Gadjah Mada, Yogyakarta,
Indonesia; 3. Interdisciplinary Program of Biomedical Sciences, Faculty of Graduate School, Chulalongkorn University,
Bangkok, Thailand; 4. Academy of Farming Brahmaputra, Yogyakarta, Indonesia.
Corresponding author: Siti Isrina Oktavia Salasia, e-mail: isrinasalasia@ugm.ac.id
Co-authors: HNP: hidayatun.nisa.purwanasari@mail.ugm.ac.id, ATUP: amandapermatasari05@gmail.com,
FBL: fajar.budi.l@mail.ugm.ac.id, MW: madarina.wasissa@mail.ugm.ac.id, KZ: khusnanzaini@gmail.com
Received: 25-01-2022, Accepted: 06-06-2022, Published online: 24-07-2022
doi: www.doi.org/10.14202/vetworld.2022.1765-1771 How to cite this article: Purwanasari HN, Permatasari ATU,
Lestari FB, Wasissa M, Zaini K, Salasia SIO (2022) Cellular immune response of Staphylococcus aureus enterotoxin
B in Balb/c mice through intranasal infection, Veterinary World, 15(7): 1765-1771.
Abstract
Background and Aim: Staphylococcus aureus produces various superantigen exotoxins, including staphylococcal
enterotoxin B (SEB). It causes fatal anaphylactic reactions and toxic shock. This study aimed to evaluate the reaction
of leukocytes and histopathological changes in the respiratory organs of Balb/c mice after intranasal infection with
enterotoxigenic S. aureus (SEB).
Materials and Methods: The presence of the seb gene in S. aureus was established in this study using polymerase chain
reaction-specific primer. Two groups of 8-week-old male Balb-c mice consist of six mice in each group. The treated group
was infected with 50 µL and 100 µL of SEB intranasal on days 1 and 14, respectively. NaCl was administered in the second
group and was considered as a control group. Blood samples were collected through the retro-orbital plexus on days 1, 4,
7, 14, and 22 after infections. Total cell counts were analyzed with an independent sample t-test and compared using the
statistical package for the social sciences (SPSS) version 16.0 (IBM Corp., NY, USA). The infected tissues of the respiratory
organ were observed descriptively and compared to the control group.
Results: The seb gene with a molecular size of 478 bp, indicating the SEB strain, is present in S. aureus used in this study.
Intranasal administration of SEB showed increased leukocytes, lymphocytes, monocytes, and eosinophils on day 22 postinfection. Significant leukocytosis was seen on days 6 and 14; lymphocytosis on days 1, 4, 6, and 16; and eosinophilia on
days 6, 14, and 22 compared with the control group (p > 0.05). In contrast, the neutrophil decreased after an increase of
immature band cells compared to the control group, indicating a severe acute infection with SEB. The lungs and trachea of
the test group had an inflammatory cell accumulation in the respiratory organ.
Conclusion: Intranasal route infection of S. aureus containing seb gene significantly induced the cellular immune response
and caused pathological changes in the respiratory tissues of the Balb/c mice model. The hematological changes were
aligned with marked pathological changes in the respiratory tract. Balb/c mice could be an excellent experimental model to
study toxic and anaphylactic shock against SEB to define the future therapeutic agents.
Keywords: enterotoxin B, hematology, histopathology, intranasal, Staphylococcus aureus.
Introduction
Staphylococcus aureus frequently colonizes
the skin and upper airways. It can be pathogenic in
several chronic airway disorders [1]. An increased
colonization rate of S. aureus in nasal polyp tissue
has been reported [2]. S. aureus can manipulate host
immune responses by producing superantigens that
facilitate invasion and colonization [3]. S. aureus
produces various superantigen exotoxins (SAEs).
Enterotoxins cause a toxic shock-like syndrome,
Copyright: Purwanasari, et al. Open Access. This article is
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food poisoning, and some allergic and autoimmune
diseases [4]. Staphylococcal enterotoxins (SEs) acting as superantigens can induce an intense T-cell
activation by releasing Type 2 cytokines. Interleukin
(IL)-4, IL-5, and IL-13 by acting on Th2 cells, can
promote a polyclonal IgE response and eosinophilic
inflammation [1, 5]. About 24 different enterotoxins
and related toxins have been described in S. aureus
with some differences in structure and biological
activity [6]. Staphylococcal enterotoxin B (SEB) is the
most potent SE since it can cause multiple organ system failure and death at even low concentrations. This
toxin is produced in large quantities by S. aureus and
is possibly the main responsible for the pathological
conditions induced by this bacterium [7]. The ability
of SEB stimulates systemic immune activation after
exposure through non-enteric mucous membranes,
primarily through the nasal tract. The nasal passage is
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the most common site of staphylococcal colonization.
Since S. aureus in the carrier state can elaborate various superantigens, there is a possibility that the nasal
passage may be exposed to SEB [8].
Animal models have great potential as powerful
tools to help answer some of the difficult questions as
human research is limited by ethical concerns and the
possibility of fatal anaphylactic reactions [9]. In vivo
animal models are important to develop therapeutics
against SEB-induced anaphylactic toxic shock. At
present, the SEB shock model requires pretreatment
with various agents to increase the sensitivity of mice
to SEB [10]. However, these models are less than
ideal, relying on artificial conditions and manipulation of the immune response. Researchers need an
excellent experimental model to address the development of a vaccine or therapy against the SEB agent. In
this study, Balb/c mice were intranasally induced with
S. aureus strain containing enterotoxin B to obtain a
natural immune response that could be an excellent
experimental model to study toxic and anaphylactic
shock against SEB to determine the future therapeutic agents. S. aureus, which contains SEB, was chosen
as an inflammatory agent in this study because SEB
is one of the SAE commonly detected in the nasal
area and has been linked to allergic diseases such as
nasal polyps or asthma. The pathogenesis of SEB that
enters the intranasal route remains unclear. Intranasal
exposure to SEB is possibly due to the colonization of
S. aureus [1, 8].
This study aimed to evaluate the cellular immune
response of Balb/c mice, including leukocyte response
and histopathological changes of respiratory organs
after being infected with enterotoxigenic S. aureus
(SEB) intranasally.
et al. [12]. The detection of enterotoxin encoding seb
gene was carried out using multiplex PCR method with
the primers, F: TCTGAACCTTCCCATCAAAAAC
and R: TCGCATCAAACTGACAAACG, and the
programs used were as follows: 35 cycles at 95°C for
15 min, 95°C for 30 s, 57°C for 90 s, 72°C for 90 s, and
72°C for 10 min.
The PCR products were analyzed by electrophoresis in 1.5% agarose gel (Invitrogen, USA) stained by
SYBR Safe (Invitrogen) in 1× TBE (Tris base, boric
acid, and ethylenediaminetetraacetic acid [EDTA])
buffer. The resulting bands were visualized on a UV
transilluminator.
SEB suspension
The molecularly confirmed SEB was subsequently cultured on blood agar (Oxoid, Germany) for
24 h at 37°C. A colony from blood agar was recultured in Todd-Hewitt broth for 24 h at 37°C. The broth
with bacterial growth was centrifuged at 1000× g for
15 min. Distilled water was added to the bacterial pellet after removing the supernatant until its turbidity
resembled a 0.5 McFarland solution (1.5 × 108 colony-forming units/mL).
Intranasal SEB challenge to animal models
Materials and Methods
Twelve 8-week-old male Balb/c mice, 20–40 g
in weight, were obtained from Integrated Research
and Testing Laboratory (LPPT), Universitas Gadjah
Mada. Mice were divided into two groups (control
and SEB test groups) to evaluate the immunogenicity.
Mice in the control group received NaCl 50 µL intranasally (i.n.) with a micropipette. Mice in the SEB test
group were intranasally administered with 50 µL and
100 µL of the bacterial suspension on days 1 and 14,
respectively. Before i.n. administration, the mice were
previously anesthetized intraperitoneal (i.p.) with the
combination of ketamine and xylazine.
Ethical approval
Hematological examinations
All procedures performed in this research were
approved by the Animal Care and Use Committee,
Faculty of Veterinary Medicine, Universitas Gadjah
Mada (No. 00114/EC-FKH/Int./2021).
Study period and location
This study was conducted from June to September
2021 at the Clinical Pathology Laboratory, Faculty of
Veterinary Medicine, Universitas Gadjah Mada.
Identification of SEB
The SEB human strain was obtained from the
Regional Health Laboratory, Yogyakarta. S. aureus containing seb gene was confirmed using polymerase chain
reaction (PCR)-specific primer. The strains have been
identified as S. aureus based on phenotypic and genotypic
identification at the Laboratory of Clinical Pathology,
Faculty of Veterinary Medicine, Universitas Gadjah
Mada. Phenotypic identifications included mannitol
salt agar, coagulase, Gram staining, and catalase [11].
Molecular identifications were performed by detecting
the 23S rRNA and nuc genes, as described by Windria
Veterinary World, EISSN: 2231-0916
Before collecting blood, mice were anesthetized
(i.p.) with a combination of ketamine and xylazine
solution. Blood samples were collected on days 1, 4,
7, 14, and 22 through the retro-orbital plexus with an
EDTA anticoagulant. Blood samples were analyzed
using a veterinary hematology analyzer (Hematology
Analyzer Mindray BC 2800 Vet, Shenzhen Mindray
Bio-Medical Electronics Co. Ltd., Shenzhen, China).
Differential leukocyte counts were manually calculated from a thin blood smear under a light microscope (Olympus, Tokyo, Japan).
Histopathological examinations
The mice were euthanized using lethal doses of
an anesthetic agent on day 22. The trachea and lungs
were collected during necropsy. The selected organs
were fixed in 10% formalin solution and were processed for standard histological preparation using
routine hematoxylin and eosin staining. The histopathological changes in the tissues were then analyzed
using a light microscope (Olympus).
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Statistical analysis
Hematology data were calculated as mean ±
standard deviation. Total blood cell counts were analyzed using an independent sample t-test and compared using SPSS version 16.0 (IBM, Armonk, USA).
The significant difference was placed at p < 0.05. The
infected tissues of the respiratory organ were descriptively observed and compared with the control group.
Results
SEB
According to the results of biochemical characteristics and amplification of the 23S rRNA in
1250 bp, nuc in 279 bp, and specific for S. aureus, the
isolate used in this study was identified as S. aureus.
The enterotoxin encoding seb gene has a molecular
size of around 478 bp (Figure-1).
Hematological examinations
Hematology examination results of both groups
were compared with the mean of all blood parameters,
as summarized in Table-1. Figure-2 shows the calculated total of leukocytes, lymphocytes, and eosinophils from days 1 to 22. Data comparisons were also
analyzed using SPSS (independent sample t-test).
Intranasal administration of SEB revealed increased
leukocytes, lymphocytes, monocytes, and eosinophils
on day 22 after infection.
The leukocyte counts in mice induced by
SEB were significantly elevated on days 6 and
14, compared to the control group (p > 0.05), followed by neutropenia with a left shift. Leukocyte
counts began to increase on 6 days post-infection
(3.75 × 103 µL−1), slightly decreased on 14 days
(3.43 × 103 µL−1), and after second i.n. SEB infection increased on day 22 (3.73 × 103 µL−1). On days
6, 14, and 22, absolute eosinophil counts were significantly elevated (p > 0.05). Eosinophils gradually
increased on 4 days after infection (1.45 × 103 µL−1)
and on 6 days (1.50 × 103 µL−1), markedly increased
on 14 days (8.52 × 103 µL−1), and, after second i.n.
SEB infection on day 22, surprisingly jumped to
59.82 × 103 µL−1, indicating severe anaphylactic
shock. The total lymphocyte counts were significantly increased on days 1, 4, 6, and 14, compared
with the control group (p > 0.5). Lymphocytes began
to increase 1 day after infection (1.77 × 103 µL−1),
peaked on 6 days (3.05 × 103 µL−1), and decreased
on 14 days (2.47 × 103 µL−1) and after the second i.n.
SEB infection increased on day 22 (3.50 × 103 µL−1).
There were no significant differences in monocyte
counts between the investigated mice. Table-2 shows
a comparison of statistical values for the total count of
leukocytes, lymphocytes, and eosinophils.
Histopathological examinations
Marked histopathological changes were found
along the respiratory tract of SEB-treated mice. An
abundant accumulation of inflammatory cells was
observed on the tracheal mucosal surface (Figure-3).
The pathological change was consistent with the
previous studies that mentioned that SEB infection causes mucosal respiratory tract damage [13].
Detailed changes are shown in Figure-4 with the accumulation of polymorphonuclear and mononuclear
inflammatory cells. Eosinophils were found within
the accumulation.
Histopathological changes were also observed
in the lower respiratory tract. Atelectasis characterized by thickening of the interstitial alveolar septa of
lungs with inflammatory cell infiltration complicated
by alveoli filled with edema fluid was also found
(Figure-5).
Discussion
Figure-1: Amplicon of the 23S rRNA (1250 bp), nuc
(279 bp), and seb gene of Staphylococcus aureus (478 bp)
and M = Marker 100 bp molecular size DNA ladder.
S. aureus used in this study contained the seb gene
with a molecular size of about 478 bp, indicating a
SEB strain. This SEB strain was isolated from humans
in Yogyakarta, Central Java, Indonesia. S. aureus containing the gene encoding SEs A, B, C, G, H, and I
have been isolated from the milk of dairy cows and
goats [11, 14]. Enterotoxins A, B, E, G, H, and I were
Table-1: Comparison of the mean blood parameters of mice after being induced with staphylococcal enterotoxin B.
Cells
Leukocyte
Lymphocyte
Eosinophil
Monocyte
Neutrophil
Control
(103 µL−1)
Day-1
(103 µL−1)
Day-4
(103 µL−1)
Day-6
(103 µL−1)
Day-14
(103 µL−1)
Day-22
(103 µL−1)
1.55
1.10
0.37
0.08
79.68
2.20
1.77
0
0.10
76.88
2.20
1.70
1.45
0.13
18.17b
3.75
3.05
1.50
0.20
27.85b
3.43
2.47
8.52
0.25
33.23b
3.73
3.50
59.82
0.30
27.91b
b
Band neutrophils observed
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Table-2: p-values obtained from the statistical package for the social sciences.
Cells
Control
(103 µL−1)
Day-1
(103 µL−1)
Day-4
(103 µL−1)
Day-6
(103 µL−1)
Day-14
(103 µL−1)
Day-22
(103 µL−1)
0.440
0.132
0.388
0.051
0.005*
0.363
0.054
0.015*
0.11
0.007*
0.007*
0.002*
0.000*
0.001*
0.004*
0.058
0.074
0.006*
Leukocyte
Lymphocyte
Eosinophil
*Significant difference (p < 0.05)
Leukocyte
90
Lymphocyte
Eosinophil
Monocyte
Neutrophil
Leukocyte (103 µL-1)
80
70
60
50
40
30
20
10
0
Control
Day-1
Day-4
Day-6
Day -14
Day -22
Leukocyte
1.55
2.2
2.2
3.75
3.43
3.73
Lymphocyte
1.1
1.77
1.7
3.05
2.47
3.5
Eosinophil
0.37
0
1.45
1.5
8.52
59.82
Monocyte
0.08
0.1
0.13
0.2
0.25
0.3
Neutrophil
79.68
76.88
18.17
27.85
33.23
27.91
Day of infection
Figure-2: Comparison of leukocytes of mice after being induced by staphylococcal enterotoxin B from day 1 until day 22.
a
b
Figure-3: The photomicrograph of mice trachea from the
(a) negative control group compared to (b) staphylococcal
enterotoxin B-infected mice that markedly showed
pathological changes with inflammatory cells accumulation
(arrow) covering alongside of tracheal surface epithelial
(H&E, ×100).
found in food products, cattle, and humans [15], in
Central Java, Indonesia, indicating the potential for
the spread of enterotoxins harmful to public health.
SEB is one of the enterotoxin proteins and is
responsible for several extensive pathophysiological changes in humans and mammals and triggers an
excessive cellular immune response leading to toxic
shock. SEBs comprise a large group of proteins and
are 19–29 kDa polypeptides in the bacterial SA protein
family [6]. SEB can activate the Toll-like receptor
2 (TLR2). TLR is essential in recognizing bacterial components to induce an appropriate immune
response against the microorganism encountered.
Bacterial SAs are a family of potent immunostimulatory exotoxins that activate T-lymphocytes. The T
Veterinary World, EISSN: 2231-0916
Figure-4: Detail magnification of mice trachea infected
by staphylococcal enterotoxin B showing the infiltration of
polymorphonuclear and mononuclear inflammatory cells,
eosinophil (arrow) (H&E, ×400).
cell receptor (TCR) molecule and the Type II major
histocompatibility complex (MHC-II) are two natural receptors that bind to staphylococcal SA. SEB can
ligate with the β-chain of TCR to induce hyperinflammatory responses and autoimmune reactions [10].
An increased presence of S. aureus enterotoxins on respiratory mucosa is linked to several diseases, including asthma, nasal polyp, and allergic
rhinitis [1]. S. aureus colonization of the nasal mucosa
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a
b
Figure-5: The photomicrograph of (a) negative control
mice lung compared to (b) staphylococcal enterotoxin
B-infected mice showed the marked changes in thickening
of interstitial alveolar-septa containing inflammatory cells
that predominantly mononuclear cells (*). Edema fluid and
inflammatory cells within alveoli were also found (H&E,
×400).
can facilitate its invasion into the subepithelial regions
where S. aureus secretes proteins that act as superantigens to activate T and B cells [13]. Bacterial superantigens are produced by S. aureus and Streptococcus
pyogenes, which are ubiquitous in nature and can
cause severe hemodynamic shock and multiorgan failure. Humans are natural carriers of these organisms,
with the nasal passage being the most common site
for S. aureus colonization. While most pathogenic isolates of S. aureus produce one or more enterotoxins,
even strains isolated from asymptomatic carriers can
produce superantigens [5, 16].
Several studies have investigated the effects of
SEs on other inflammatory cells such as eosinophils,
macrophages, and mast cells, although SEs mainly
affect lymphocyte activation. It has been shown that
SEs can promote eosinophils’ survival by inhibiting
eosinophil apoptosis [17]. In addition, SEs can act on
macrophages by inducing the production of cytokines
such as IL-8 and IL-12 and neutrophilic chemotactic
factors [1]. S. aureus protein A can induce cross-linking of IgE molecules in mast cells, which increases the
release of histamine, tryptase, and leukotriene C4 [18].
S. aureus containing seb gene encoding SEB used
in this study changed the cellular immune response
with increase in leukocytes, lymphocytes, monocyte,
and eosinophils on day 6 post-infection (Table-1). The
total leukocytes of the SEB-induced mice were significantly increased compared with the control group
on days 6 and 14 (p < 0.05) followed by neutropenia with a left shift. Intranasal administration of SEB
caused a significant increase in leukocytes in all the
mice investigated (Figure-2). Leukocyte changes and
their differences are used as an indicator of the body’s
immune system response to pathogens. The increase
in total leukocytes correlates with an increase in the
number of cells produced by the bone marrow and
their migration from the circulation to the tissues [19].
SEBs have the ability to cause systemic immune
activation after exposure through the nasal tract [8].
Neutropenia with a left shift indicated the severity of
acute SEB infection. Neutrophils are needed to phagocyte the bacteria in the nasal tract. Neutrophils respond
to bacterial respiratory tract infections and colonize
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respiratory tissues. Consequently, neutrophils seem to
be reduced in circulation. This condition stimulated
the bone marrow to release young neutrophils (band
cells), resulting in neutropenia with a left shift [20].
The total eosinophil counts showed a significant
increase in eosinophils (eosinophilia) (Figure-1) on
days 6, 14, and 22 (p > 0.05), particularly after SEB
infection on day 22, indicating severe anaphylactic
shock. These data correspond to a previous study by
Hellings et al. [21]. S. aureus is capable of producing
25–30 kDa exotoxin, one of which is SE with the gene
seb. SEB can increase the potential for allergies, such
as skin inflammation, increased eosinophils in models affected by allergic rhinosinusitis, and polypoid
nasal lesions [22]. SEB promotes the release of Type 2
cytokines IL-4 and IL-13 by acting on Th2 cells and
promoting eosinophilic infiltration [5]. SEB also
mediated eosinophil influx because higher IL-5 level
leads to enhanced eosinopoiesis and bronchial influx
of eosinophils [21]. The number of eosinophils in the
circulating blood increases in the late stages of allergic
inflammation and usually remains high compared to
the inflammatory cells themselves [23]. Eosinophils
are chemotactic cells that migrate from the bone marrow into the bloodstream and end up in inflamed tissues. Therefore, eosinophil chemotaxis is important as
a target for anti-allergic drugs. Eosinophil activation
through different surface receptors allows the release
of mediators such as lipids and cytokines through
different mechanisms such as exocytosis, gradual
degranulation, and cytolysis [24].
The results of the lymphocyte examination show
that the number of lymphocytes increased (lymphocytosis) significantly after induction with SEB compared to the control group starting from day 6. An
increase in lymphocytes is needed in bacterial infections to assist in the production of lymphokines that
act as chemoattractants to stimulate the emergence of
cellular immunity in the body [19]. Monocytes also
doubled by day 6 and continued to increase through
day 22. Bacterial superantigens can upregulate TLR
expression in primary human monocytes by ligation
of MHC Class II [25].
The pathogenic mechanism of SEB causing
respiratory disorder remains unclear. Therefore, an
investigation of the detailed pathological changes is
needed to understand its pathogenicity. This study
found marked pathological changes in the trachea,
particularly along the epithelial surface. The result
agrees with the previous study that described complex immune regulations during SEB infection that
resulted in nasal epithelial damage [13].
Several pathological changes occurred in the
lungs, such as thickening alveolar septa with inflammatory cells, edema fluid, and inflammatory cells
within the alveoli. Along the trachea, there was also
an accumulation of inflammatory cells. Intranasal
inoculation of S. aureus containing SEB caused trachea and lung inflammation and systemic immune
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system activation. In addition, nasal SEB increased
the bronchial expression of eotaxin-1, which acts synergistically with IL-5 to recruit eosinophils from the
blood to the inflamed airways [26]. Pro-inflammatory
cytokines and chemokines, which are inflammatory mediators, can be produced in response to SEs.
These inflammatory mediators can cause leukocyte
migration and tissue damage. These inflammatory
mediators cause a hyperacute release of the cytokines
TNF-α, IL-1 and IL-2, IL-10, IFN-γ, monocyte chemoattractant protein-1 (MCP-1), and others derived
from T cells.
SE has an exotoxin capable of bypassing normal
antigen-processing mechanisms and binds to MHC-II
molecules on antigen-presenting cells and V regions.
SEs can activate and stimulate T-cell formation,
which is then referred to as superantigens. The ability of superantigen affinity allows microbes to excrete
toxins, disrupt the body’s defense system, increase
pro-inflammatory cytokines, chemokines, and lytic
enzymes, and activate inflammatory and coagulation
processes. T-helper 1 cells work together with TNF
and IL-1 to trigger immune reactions and tissue damage. IL-2, as a result of the activation of superantigens
by T cells, causes vasodilation and damage to blood
vessels leading to edema. Chemokines, MCP-1, and
the presence of IL-8 and macrophage inflammatory
protein-1α, which are the result of direct induction by
SE, cause the migration of leukocytes, neutrophils,
and dendritic cells to infected tissues [10, 20].
Cellular immune response studies in the Balb/c
mouse model describe the clinicopathological changes
caused by enterotoxigenic S. aureus infection [27].
Lestari et al. [28] have also reported resistance of
enterotoxin-containing S. aureus to the cellular
immune defense system.
SIOS: Conceptualized and supervised the study and
drafted the manuscript. All authors have read and
approved the final manuscript.
Acknowledgments
This study was funded by a grant from the
Ministry of Education, Technology, and Research of
the Indonesian Government (Grant no. 1653/UN1/
DITLIT/DIT-LIT/PT/2021).
Competing Interests
The authors declare that they have no competing
interests.
Publisher’s Note
Veterinary World remains neutral with regard
to jurisdictional claims in published institutional
affiliation.
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Conclusion
It can be concluded that infection of S. aureus
containing enterotoxin B, through the intranasal route
of Balb/c mice, could significantly induce the cellular immune response, marked by increasing the leukocytes’ lymphocytes, monocytes, and eosinophils
and decreasing the neutrophil with immature band
cells. Eosinophil findings might correlate to the allergic response due to SEB infection. The pathological
changes in the respiratory tract were correlated with
the hematological changes. To study toxic and anaphylactic shock against SEB, and determine future
therapeutic agents, Balb/c mice could be an excellent
experimental model.
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Authors’ Contributions
HNP: Performed the experiment, data analysis, and drafted the manuscript. ATUP: Performed
the experiment, data analysis and reviewed the
manuscript. FBL: Data analysis and drafted the manuscript. MW: Data analysis and reviewed the manuscript. KZ: Supervised and reviewed the manuscript.
Veterinary World, EISSN: 2231-0916
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