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Assessing Humoral and Cellular Immunity in a Rat Model of Staphylococcal Bacterial Pneumonia

Penilaian Imunitas Humoral dan Seluler pada Model Tikus Pneumonia Bakteri Staphylococcus
Vol. 2 No. 2 (2025): Oktober:

Wasan Abdulateef Majeed (1), Ola Abdulkareem Kadhim (2), Zainab Hussein Mahdi (3)

(1) Department of Biology, College of Education for Pure Science, University of Diyala, Iraq
(2) Department of Biotechnology, College of Science, University of Anbar, Iraq
(3) Department of Biology, College of Education for Pure Science, University of Diyala, Iraq
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Abstract:

General Background: Staphylococcus aureus pneumonia remains a major global health concern due to its virulence, biofilm formation, and rising methicillin-resistant strains, which complicate treatment. Specific Background: Understanding the interplay between humoral and cellular immunity is crucial for designing effective interventions, as both antibody-mediated and T-cell–mediated responses contribute to pathogen clearance. Knowledge Gap: While immune evasion strategies of S. aureus are documented, quantitative insights into the temporal dynamics of antibody production, T-cell proliferation, and cytokine release during infection are limited. Aims: This study aimed to evaluate the kinetics of humoral and cellular immune responses in a rat model of S. aureus pneumonia. Results: Infected rats exhibited significantly elevated IgM and IgG levels, with IgM peaking at day 14 and IgG progressively increasing. Splenocyte proliferation and cytokine production (IFN-γ, IL-4) were markedly enhanced, particularly at day 21, indicating strong Th1 and Th2 activation. Novelty: The study provides an integrated temporal profile of dual-arm immunity in experimental S. aureus pneumonia, demonstrating concurrent robust humoral and cellular activation. Implications: These findings highlight the necessity of targeting both antibody and T-cell responses in vaccine design, potentially guiding the development of immunotherapies for effective prevention and treatment of S. aureus pneumonia.
Highlight :



  • IgM peaked on day 14, while IgG continued to rise until the end of the study.

  • Splenocyte proliferation indicated strong T cell activation.

  • Th1 and Th2 responses worked together to eliminate S. aureus from the lungs.


Keywords : Staphylococcus, Humoral, Cellular, Immunity, Rat Model

References

[1] D. Parker, C. L. Ryan, F. Alonzo, V. J. Torres, P. J. Planet, and A. S. Prince, “CD4+ T Cells Promote the Pathogenesis of Staphylococcus Aureus Pneumonia,” J. Infect. Dis., vol. 211, no. 6, pp. 835–845, 2015, doi: 10.1093/infdis/jiu525.

[2] J. Braverman, I. R. Monk, C. Ge, et al., “Staphylococcus Aureus Specific Lung Resident Memory CD4+ Th1 Cells Attenuate the Severity of Influenza Virus Induced Secondary Bacterial Pneumonia,” Mucosal Immunol., vol. 15, no. 4, pp. 783–796, 2022, doi: 10.1038/s41385-022-00529-4.

[3] W. H. Self, R. G. Wunderink, D. J. Williams, et al., “Staphylococcus Aureus Community-Acquired Pneumonia: Prevalence, Clinical Characteristics, and Outcomes,” Clin. Infect. Dis., vol. 63, no. 3, pp. 300–309, 2016, doi: 10.1093/cid/ciw300.

[4] L. Hall-Stoodley, J. W. Costerton, and P. Stoodley, “Bacterial Biofilms: From the Natural Environment to Infectious Diseases,” Nat. Rev. Microbiol., vol. 2, no. 2, pp. 95–108, 2004, doi: 10.1038/nrmicro821.

[5] N. J. Verkaik, C. P. de Vogel, H. A. Boelens, et al., “Anti-Staphylococcal Humoral Immune Response in Persistent Nasal Carriers and Noncarriers of Staphylococcus Aureus,” J. Infect. Dis., vol. 199, no. 5, pp. 625–632, 2009, doi: 10.1086/596743.

[6] F. Askarian, T. Wagner, M. Johannessen, and V. Nizet, “Staphylococcus Aureus Modulation of Innate Immune Responses Through Toll-Like (TLR), NOD-Like (NLR) and C-Type Lectin (CLR) Receptors,” FEMS Microbiol. Rev., vol. 42, no. 5, pp. 656–671, 2018, doi: 10.1093/femsre/fuy025.

[7] J. S. Cho, Y. Guo, R. I. Ramos, et al., “Neutrophil-Derived IL-1β Is Sufficient for Abscess Formation in Immunity Against Staphylococcus Aureus in Mice,” PLoS Pathog., vol. 8, no. 11, p. e1003047, 2012, doi: 10.1371/journal.ppat.1003047.

[8] L. S. Miller, V. G. Fowler, S. K. Shukla, et al., “Development of a Vaccine Against Staphylococcus Aureus Invasive Infections: Evidence Based on Human Immunity, Genetics and Bacterial Evasion Mechanisms,” FEMS Microbiol. Rev., vol. 44, no. 1, pp. 123–153, 2020, doi: 10.1093/femsre/fuz030.

[9] A. F. Brown, J. M. Leech, T. R. Rogers, and R. M. McLoughlin, “Staphylococcus Aureus Colonization: Modulation of Host Immune Responses and Impact on Human Vaccine Design,” Front. Immunol., vol. 4, p. 507, 2013, doi: 10.3389/fimmu.2013.00507.

[10] Y. Wang, L. I. Cheng, D. R. Helfer, et al., “Mouse Model of Hematogenous Implant-Related Staphylococcus Aureus Biofilm Infection Reveals Therapeutic Targets,” Proc. Natl. Acad. Sci. U. S. A., vol. 114, no. 26, pp. E5094–E5102, 2017, doi: 10.1073/pnas.1703427114.

[11] D. Nurjadi, M. Kain, P. Marcinek, et al., “Ratio of T-Helper Type 1 (Th1) to Th17 Cytokines in Whole Blood Is Associated With Human β-Defensin 3 Expression in Skin and Persistent Staphylococcus Aureus Nasal Carriage,” J. Infect. Dis., vol. 214, no. 11, pp. 1744–1751, 2016, doi: 10.1093/infdis/jiw440.

[12] A. K. Varshney, G. A. Kuzmicheva, J. Lin, et al., “A Natural Human Monoclonal Antibody Targeting Staphylococcus Aureus Toxins Protects Against Pneumonia and Skin Infection,” mBio, vol. 9, no. 6, p. e02391-18, 2018, doi: 10.1128/mBio.02391-18.

[13] A. Nakou, M. Woodhead, and A. Torres, “MRSA as a Cause of Community-Acquired Pneumonia,” Eur. Respir. J., vol. 34, no. 5, pp. 1013–1014, 2009, doi: 10.1183/09031936.00120009.

[14] P. Matzinger, “The Danger Model: A Renewed Sense of Self,” Science, vol. 296, no. 5566, pp. 301–305, 2002, doi: 10.1126/science.1071059.

[15] J. K. Rudkin, A. M. Edwards, M. G. Bowden, et al., “Methicillin Resistance Reduces the Virulence of Healthcare-Associated Methicillin-Resistant Staphylococcus Aureus by Interfering With the Agr Quorum Sensing System,” J. Infect. Dis., vol. 205, no. 5, pp. 798–806, 2012, doi: 10.1093/infdis/jir845.

[16] P. Peyrani, M. Allen, T. L. Wiemken, et al., “Severity and Outcomes of Adults Hospitalized With Laboratory-Confirmed Influenza: The Hospitalized Influenza Adults (HIA) Project,” BMC Infect. Dis., vol. 19, no. 1, p. 89, 2019, doi: 10.1186/s12879-019-3729-5.

[17] S. A. Fritz, K. M. Tiemann, P. G. Hogan, et al., “A Serologic Correlate of Protective Immunity Against Community-Onset Staphylococcus Aureus Infection,” Clin. Infect. Dis., vol. 56, no. 11, pp. 1554–1561, 2013, doi: 10.1093/cid/cit123.

[18] A. S. Anderson, I. L. Scully, Y. Timofeyeva, et al., “Staphylococcus Aureus Manganese Transport Protein C Is a Highly Conserved Cell Surface Protein That Elicits Protective Immunity Against S. Aureus and Staphylococcus Epidermidis,” J. Infect. Dis., vol. 205, no. 10, pp. 1688–1696, 2012, doi: 10.1093/infdis/jis278.

[19] R. A. Proctor, “Is There a Future for a Staphylococcus Aureus Vaccine?,” Vaccine, vol. 30, no. 19, pp. 2921–2927, 2012, doi: 10.1016/j.vaccine.2011.11.006.