In the last two blogs, we saw how the biofilms are formed and how they escape the antibiotic attack. In this blog, we shall see the ways by which the biofilm can escape the attack by the host’s immune system…
Biofilms avoid the evasion by host’s immune system by different ways. Few of them are:-
1. Concealing the surface molecules:
The immune system can initiate the immune response only after the pathogen is recognised. (Read more on antigen recognition here). The immune system senses the pathogen by the different patterns, molecules and antigen on the bacterial molecules cell surface. In the biofilm, these entities are concealed by the extracellular polymeric sucstance (EPS) or the matrix of the biofilm. Hence, one of the early and important step of antigen recognition, itself is hindered.
2. Restricting the movement of immune cells:
The EPS is made up of different components like charged polysaccharides, proteins, lipids, water and nucleic acids, which gives it a gel-like constituency. These charges and molecules make the penetration and the movement of the immune cells into the biofilm difficult. The phagocytes like PMN and macrophages are hence unable to clear the bacteria protected within the cover of the matrix.
The matrix also hinders the movement of various molecules important for immune response. For example, IgG and complement components are unable to enter and bind the bacterial cells, hence avoiding opsonization and activation of complement pathway.
3. Impaired phagocytosis:
EPS not only hampers the movement but also the process of phagocytosis by the phagocytes like macrophage and neutrophils.
Phagocytosis by neutrophils is impaired as seen in S. pneumoniae biofilms. They undergo frustated phagocytosis. That is as the phagocytosis of the cells become difficult due to the gluey EPS, the neutrophils begin to release the potent components like Antimicrobial peptides (AMPs), Reactive oxygen species (ROS) and other cytotoxic and proinflammatory substances around the biofilm. These potent substances effects only the outermost layer of the biofilm and also the host tissue surrounding it Hence causing more harm to the host than the biofilm.
(Just for info: Watch this amazing video on frustrated phagocytosis by PLoS Media).
Biofilm can cause change in phenotype of macrophage from M1 to M2. M1 macrophages are cytotoxic [secrete high levels of proinflammatory cytokine (IL-12) and low levels of anti inflammatory cytokines (IL-10)]. M2 are the resident macrophages, which are involved in functions like wound healing and tissue repair and produce anti-inflammatory cytokines like IL-10.
Hence the macrophages invading the biofilm cause low level of phagocytosis as they are skewed toward M2 phenotype.
E.g. The Methicillin-resistant Staphylococcus aureus (MRSA) biofilm bacteria avoid being killed by macrophage (M1 phenotype).
(Just for info: Read a paper).
4. Phenotypic switching:
The bacteria in biofilm has a repertoire of genetic advantages. One such advantage is the ability to exhibit a different subset of antigens, that is antigenic variation. In this the bacteria alters the surface proteins and escapes the host immune response, as the immune system reacts to antigens it recognises.
E.g. Phenotypic variation in multiple Staphylococcus epidermidis isolates has been observed. (Read the paper).
Hence the biofilm tricks the immune system and continues to thrive within the host and cause some very serious health problems. We shall discuss a few of these diseases, in the next post.
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Ref (fig):
– Schinwald & Donaldson (2012) Use of back-scatter electron signals to visualise cell/nanowires interactions in vitro and in vivo; frustrated phagocytosis of long fibres in macrophages and compartmentalisation in mesothelial cells in vivo. Particle and fibre toxicology. 9:34.
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