Strategies Used by Microbiological Pathogens to Evade Host Immunity

Jacek Lamarca^*
*Correspondence: Jacek Lamarca, Department of Genetics and Microbiology, Institute of Biological Sciences, Maria Curie-Skłodowska University, Akademicka, Poland, Email:

Keywords

Host immune evasion • Microbial pathogens • Antigenic variation • Immune modulation Phagocytosis • Complement activation • Infectious diseases

Introduction

Infectious diseases caused by microbial pathogens remain a significant global health concern. These pathogens have evolved intricate mechanisms to overcome and manipulate the host immune system, facilitating their survival and proliferation within the host. By evading immune defenses, pathogens can establish chronic or recurrent infections, leading to a multitude of clinical manifestations. Understanding the strategies employed by microbial pathogens to subvert the host immune response is crucial for the development of effective therapeutic interventions. In this article, we will delve into the fascinating world of host immune evasion and discuss key strategies employed by microbial pathogens.

One of the most potent strategies employed by pathogens is antigenic variation. By altering their surface antigens, pathogens can evade recognition by the host immune system. This phenomenon is commonly observed in pathogens such as the influenza virus, P. falciparum (malaria parasite) and T. brucei (causative agent of African sleeping sickness). Through genetic mutations or recombination events, pathogens can generate a diverse repertoire of antigenic variants, rendering the host immune response less effective. This constant antigenic variation poses a significant challenge for the development of effective vaccines, as immunity against one variant may not provide protection against others. Microbial pathogens can also manipulate the host immune response by altering immune signaling pathways or suppressing immune cell functions. For instance, viruses like Human Immunodeficiency Virus (HIV) and Herpes Simplex Virus (HSV) have evolved mechanisms to downregulate Major Histocompatibility Complex (MHC) molecules, impairing antigen presentation and T-cell recognition. Additionally, certain bacteria, such as Mycobacterium tuberculosis, can inhibit phagosome-lysosome fusion, allowing them to survive and replicate within macrophages. These immune modulation strategies enable pathogens to evade detection and clearance by the immune system, thereby establishing chronic infections [1,2].

Literature Review

Ingenious techniques have been developed by microbial pathogens to subvert and control the immune response of the host. Pathogens can successfully establish infections and avoid immune clearance by using strategies such antigenic variation, immunological modulation, subversion of phagocytosis and suppression of complement activation. The development of efficient treatment approaches, like as vaccinations and innovative antibacterial techniques, depends on understanding these evasion techniques. We can improve our capacity to fight infectious illnesses and protect public health in the face of emerging microbial threats by unravelling the complex host-pathogen interactions.

Phagocytosis is a critical immune mechanism by which pathogens are engulfed and destroyed by phagocytic cells, such as macrophages and neutrophils. However, microbial pathogens have developed various mechanisms to evade or subvert phagocytosis. Some bacteria produce capsules that hinder phagocytic engulfment, while others secrete toxins that kill phagocytes or inhibit phagosome maturation. Additionally, certain pathogens, including the protozoan parasite T. gondii, can manipulate host cell actin to facilitate their own entry and subsequent replication. By subverting phagocytosis, pathogens can evade immune surveillance and establish successful infections. The complement system is a crucial component of the innate immune response, providing rapid defense against invading pathogens. However, many microbial pathogens have developed strategies to inhibit complement activation. For example, some bacteria produce surface proteins that bind and inactivate complement components, while others express molecules that mimic host regulators of complement activation, thereby preventing complement-mediated killing. By inhibiting complement activation, pathogens can evade an important arm of the immune system and enhance their survival within the host [2,3].

The study of host immune evasion strategies employed by microbial pathogens is an active area of research, driven by the need to develop effective treatments and preventive measures against infectious diseases. By gaining a deeper understanding of these mechanisms, researchers can identify vulnerabilities in the pathogens' evasion strategies and exploit them for therapeutic purposes. Continued research efforts should focus on identifying new and previously unknown immune evasion strategies employed by microbial pathogens. Advancements in technologies such as genomics, proteomics and high-throughput screening have enabled researchers to uncover novel evasion mechanisms. Identifying these mechanisms will provide valuable insights into the complex interactions between pathogens and the host immune system, leading to the development of innovative therapeutic interventions. Once evasion mechanisms are identified, efforts can be directed towards developing strategies to disrupt or inhibit key molecules involved in the immune evasion process. For example, monoclonal antibodies can be designed to specifically target and neutralize pathogen-derived molecules that interfere with immune signaling or inhibit complement activation. This approach has shown promise in the development of therapeutics against pathogens such as HIV and Ebola virus [4,5].

Discussion

Understanding how pathogens employ antigenic variation to evade immune recognition is crucial for the development of effective vaccines. By identifying conserved regions or targeting multiple variants, researchers can design vaccines that induce broad and long-lasting immune responses. Additionally, incorporating adjuvants or delivery systems that enhance antigen presentation and immune activation can further improve vaccine efficacy. Combining multiple therapeutic approaches may be necessary to overcome the complex immune evasion strategies employed by pathogens. For instance, combining vaccines that induce strong and diverse immune responses with immune checkpoint inhibitors or immunomodulatory agents could enhance the host immune response against pathogens that manipulate or suppress immune cells. Such combination therapies have shown promise in cancer immunotherapy and could potentially be adapted for infectious diseases as well. In addition to targeting the pathogens directly, host-directed therapies aim to modulate the host immune response to enhance pathogen clearance. By boosting innate immune responses or modulating immune signaling pathways, host-directed therapies can potentially counteract the immune evasion strategies employed by pathogens. However, careful consideration must be given to avoid excessive immune activation or disruption of normal immune functions [6].

Conclusion

Microbial pathogens have evolved diverse and intricate strategies to evade and manipulate the host immune response. Understanding these evasion mechanisms is crucial for developing effective therapeutic interventions against infectious diseases. Ongoing research efforts focused on unraveling the complex interactions between pathogens and the host immune system will provide valuable insights and pave the way for the development of novel treatment strategies, vaccines and host-directed therapies. By combating the immune evasion strategies employed by microbial pathogens, we can significantly improve our ability to control and prevent infectious diseases, safeguarding public health worldwide.

Acknowledgement

We thank the anonymous reviewers for their constructive criticisms of the manuscript.

Conflict of Interest

The author declares there is no conflict of interest associated with this manuscript.

References

1. Silhavy, Thomas J., Daniel Kahne and Suzanne Walker. "The bacterial cell envelope." Cold Spring Harb perspect biol 2 (2010): a000414.

Google Scholar, Crossref, Indexed at

2. Chachaj-Brekiesz, Anna, Jan Kobierski, Anita Wnętrzak and Patrycja Dynarowicz-Latka. "Electrical properties of membrane phospholipids in Langmuir monolayers." Membr 11 (2021): 53.

Google Scholar, Crossref, Indexed at

3. Leekumjorn, Sukit and Amadeu K. Sum. "Molecular simulation study of structural and dynamic properties of mixed DPPC/DPPE bilayers." Biophys J 90 (2006): 3951-3965.

Google Scholar, Crossref, Indexed at

4. Emens, Leisha A. and Gary Middleton. "The interplay of immunotherapy and chemotherapy: Harnessing potential synergies." Cancer Immunol Res 3 (2015): 436-443.

Google Scholar, Crossref, Indexed at

5. Ley, Ruth E., Daniel A. Peterson and Jeffrey I. Gordon. "Ecological and evolutionary forces shaping microbial diversity in the human intestine." Cell 124 (2006): 837-848.

Google Scholar, Crossref, Indexed at

6. Zheng, Danping, Timur Liwinski and Eran Elinav. "Interaction between microbiota and immunity in health and disease." Cell Res 30 (2020): 492-506.

Google Scholar, Crossref, Indexed at