Bacterial Evasion of Host Immune System

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BACTERIAL EVASION OF HOST IMMUNE SYSTEM

A host is usually colonised by commensals bacteria, most of which form the normal flora. These bacteria do not harm to the host and can even be beneficial under some circumstances. On the other hand, certain bacteria can cause diseases and they are referred to as pathogens. When pathogenic bacteria infect a host, they make use of their virulence mechanisms to fight the host’s innate and adaptive immune systems, the result of which can lead to diseases.

To be able to cause disease, many pathogens depend on their ability to invade a host and resist or counteract the latter’s immune defence. Successful pathogens have evolved several anti-immune strategies which allow them to evade the host’s immune defences and they do so by interfering with the immune system, hiding from the latter or destroying elements of the immune system [1]. Table 1.0 summarises the mechanisms adopted by pathogens to evade the immune system.

Table 1.0: Some major mechanisms adopted by bacteria to evade the immune system

Mechanisms

Example

Use of secretions

  • Toxins
  • Proteins
  • Enzymes

Pathogens make use of modulators on their surfaces

  • Lipid A on Gram negative’s cell walls
  • Capsules
  • Invasins

Antigenic variation

  • Change in their surface receptors to avoid humoral immune response

Avoid/evade/survive phagocytosis

  • Escape phagocytosis
  • Inhibit phagocyte maturation
  • Avoid phagolysosome formation
  • Destroy phagocytes

By blocking the acquired immunity

  • Block the antigen presentation process
  • Down-regulate activity of MHC II
  • Destroy antibodies
  • Destroy effector T cells

Inhibit complement activity

  • Release proteases to degrade complement proteins

Cytokine release

  • Block inflammatory pathway
  • Suppress T cells proliferation

Evasion of the innate immune system

  1. Use of secretions

Most of the pathogens are intracellular. However, extracellular pathogens do not need to invade the host to cause diseases. They can do so by using several secretion processes, thereby delivering toxins and other virulence components into the host cells, destroying immune cells [2]. Some bacteria, including E.coli and Y.pestis, can develop a translocon, which upon contact with a host cell allow them to deliver their virulence components into the cells, resulting in apoptosis. B.pertussis can release toxins which lead to ciliostatsis, allowing the pathogen to enter the cells [2].

Some pathogens are also well known for releasing proteins. For example, B.anthracis secretes a protective antigen which upon binding to host cell receptors, allow the entry of a lethal or edema factor. S.aureus can produce the coagulase enzyme which converts fibrin to fibrinogen, leading to the formation of a clot-like barrier, protecting the bacteria from immune response [2].

  1. Use of capsules

Both Gram positive and Gram negative bacteria need to hide their surface carbohydrates and proteins from immune responses and at the same time expose their invasins. The best way to achieve this is by expressing capsules. Made of polysaccharides, capsules are poorly immunogenic and therefore help shield the bacteria from the immune responses [2]. For example, the capsule of S.pyogenes which is made up of hyaluronic acid resembles the connective tissues in human and can therefore prevent recognition of the bacteria by the host’s immune system [2]. Capsules, being slimy, also help the pathogen in escaping phagocytosis. As shown in figure 1.0, S.aureus can produce protein A, which helps the latter to inhibit the binding of antibody receptors, thereby decreasing the performance of opsonins [3].

Figure 1.0: Opsonisation inhibition by S.aureus

  1. Phagocytosis evasion

Phagocytosis is one of the most important ways of eliminating microbes. However, many pathogens have developed ways to evade phagocytes, survive within the latter if engulfed and escape killing by the latter [3]. Some bacteria have the ability of supressing the inflammatory response and interfering with chemotaxis, thereby preventing the phagocytes from reaching the sites of infection. Some bacteria can even display factors, allowing them to present themselves as ‘self’ and thereby avoiding the phagocytes. T.pallidum, for example, is able to cause syphilis by coating itself with fibronectin, a compound produced by the body [3]. Yersinia species have a type III secretion system which allows them to inject several effectors, leading to a neutralisation in phagocytic activity [4].

However, if they did not manage to escape the phagocytes, some bacteria can still survive within phagocytes [5]. Bacteria like M.tuberculosis can prevent the formation of the phagolysosome, using an array of effector molecules. Other pathogen like L.pneumophila releases secretions that induce the fusion of the phagosome with vesicles other than the lysosome. L.monocytogenes can even escape from the phagocyte before the fusion of the phagosome and the lysosome by producing listeriolysin O, which lyse the phagosome and using actins to spread to neighbouring cells [3][6].

Resistance to the adaptive immune system

Once they have escaped killing by the phagocytes, pathogens employ other mechanisms to evade the adaptive immunity as well. They prevent activation of the adaptive immune system by affecting cytokine secretion, antigen presentation and proliferation of effector cells [6].

  1. Induction of immunosuppressive cytokines

Some bacteria can produce anti-inflammatory cytokines, which suppress the release of cytokines, leading to a decline in the activity of phagocytes and other effector cells [6]. Mycobacterium for example can release IL-6 and IL-10 which prevent T cells and macrophages activation, respectively [6].

  1. Interference with APCs

Bacteria like H.pylori have the ability to inhibit the degradation of antigen by the APCs and affect presentation on MHC II. M.tuberculosis can also interfere with antigen presentation by MHC II since they are able to down-regulate the latter [6].

  1. Inhibition of the T and B cells functions

Bacteria employ several mechanisms to evade the humoral immunity. Bacteria like S.pneumoniae and N.gonorrhoeae can secrete IgA proteases which inactivate the IgA antibody secreted. The protein A secreted by S.aureus can inactivate IgG antibodies [7]. Also, some bacteria coat themselves with self-compounds so that antibodies are not produced against them.

Many pathogens make use of genetic mechanism to generate antigenic variation, thereby escaping recognition by the immune cells and the antibodies. Antigenic variation usually occurs by 3 different mechanisms. Firstly, some bacteria have different copies of a single molecule and each of them switch on and off independently. Secondly, some bacteria possess one expression locus together with several silent genes and can change which gene is to be expressed. Thirdly, some genome has variable regions which keep on changing [8]. S.pnemoniae for example, has a large diversity of serotype, each expressing a different polysaccharide capsule [7]. Neisseria species on the other hand can make use of the 3 mechanisms to induce genetic variation, making it difficult to treat infections caused by this pathogen [9].

Bacteria can also inhibit the activation and action of effector T cells. H.pylori for example can secrete a toxin which blocks T cells proliferation. The Opa protein produced by N.gonorrhoeae can bind to a receptor expressed on T helper cells and thereby suppressing their proliferation [10].

For a bacterium to become a successful pathogen, it must be able to overcome the effective innate and adaptive host defences. While some pathogens possess single virulence factors, others like S.aureus have multiple virulence mechanisms which allow the latter to invade the host.

Word count: 1060

REFERENCES

  1. Williamson D. Host− Pathogen interactions and immune evasion. British society for Immunology. Accessed on: 10 November 2014.

Available from: http://bitesized.immunology.org/pathogens-and-disease/host%E2%88%92pathogen-interactions-and-immune-evasion

  1. Finlay B.B. and McFadden G., 2006. Anti-Immunology: Evasion of the Host Immune System by Bacterial and Viral Pathogens. Cell, 124(4), 767-782.
  1. Boundless. Microbial Evasion of Phagocytosis, 2014. Boundless Anatomy and Physiology. Accessed on: 10 November 2014

Available from: https://www.boundless.com/physiology/textbooks/boundless-anatomy-and-physiology-textbook/the-immune-system-21/immune-system-disorders-and-clinical-cases-204/microbial-evasion-of-phagocytosis-999-1226/

  1. Mota L.J., Cornelis G.R., 2005. The bacterial injection kit: type III secretion systems. Annual Medicine, 37, 234–249.
  1. Rosenberger C.M., Finlay B.B., 2003. Phagocyte sabotage: disruption of macrophage signalling by bacterial pathogens. Nat. Rev. Mol. Cell Biol., 4, 385–396.
  1. Janeway C.A Jr, et al., 2001. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science.

Accessed on: 10 November 2014

Available from: http://www.ncbi.nlm.nih.gov/books/NBK27176/

  1. Hornef M.W., Wick M.J., Rhen M., Normark S., 2002. Bacterial strategies for overcoming host innate and adaptive immune responses. Nature immunology, 3(11), 1033-1040.
  1. Finlay B.B, Falkow S., 1997. Common themes in microbial pathogenicity revisited. Microbiol. Mol. Biol. Rev., 61, pp. 136–169.
  1. Todar K. Bacterial Defense against Specific Immune Responses. Todar’s online textbook of bacteriology. Accessed on: 10 November 2014

Available from:http://textbookofbacteriology.net/antiimmuno.html

  1. Boulton I.C., Gray-Owen S.D., 2002. Neisserial binding to CEACAM1 arrests the activation and proliferation of CD4+ T lymphocytes. Nat. Immunol., 3, pp. 229–236

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