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Review
. 2009 Apr;30(11):1989-2005.
doi: 10.1016/j.biomaterials.2008.11.025. Epub 2009 Jan 29.

Biomimetic strategies based on viruses and bacteria for the development of immune evasive biomaterials

Matthew T Novak  1 , James D Bryers, William M Reichert
Affiliations
Review

Biomimetic strategies based on viruses and bacteria for the development of immune evasive biomaterials

Matthew T Novak et al. Biomaterials. 2009 Apr.

Abstract

The field of biomaterials has begun to focus upon materials strategies for modulating the immune response. While certain approaches appear promising, they are currently limited to isolated facets of inflammation process. It is well documented that both bacteria and viruses have highly developed methods for evading the immune system, providing inspiration for a more biomimetic approach to materials design. This review presents the immune evasive tactics employed by viruses and bacteria, and offers suggestions for future directions that apply these principles to design of immune evasive biomaterials.

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Figures

Figure 1
Figure 1
Diagram of differentiation of macrophage phenotypes. M1 activation represents classical activation and production of pro-inflammatory cytokines. M2 activation may take on three different forms. All three share the properties of being either immunosuppressive or immunoregulatory in nature. Figure adapted from [8].
Figure 2
Figure 2
Schematic of how HIV may both interrogate a host cell and incorporate host-derived proteins onto its surface. The gp120 receptor on the HIV virion binds preferentially to CD4 receptors on the host and the viral cargo is transmitted to the host through the gp120/CD4 complex. During the budding process, the virion can incorporate host-derived proteins on the cell surface, thereby providing itself with camouflage to disguise itself against immune response. Figure modified from [137].
Figure 3
Figure 3
Schematic of viral immune evasive secretions. a: Schematic of cytokine inhibition by viral proteins. Cowpox virus encodes for CrmA, preventing cleavage of pro IL-1β to IL-1β. b: The generation of vIL-10 from viruses activates JAK/STAT, p38 and MAP kinase pathways, producing carbon monoxide. It is believed that carbon monoxide is the agent that blocks transcription of pro-inflammatory cytokines. c: The complexation of a pro-inflammatory cytokine with a virally derived receptor homologue will prevent cytokine binding and activation of pro-inflammatory pathways in surrounding cells. d: Viruses incorporate host derived proteins like CD59 that will inhibit complementary response.
Figure 4
Figure 4
Transmission electron micrographs of Staphylococcus haemolyticus. a: Visualization of the bacterial capsule formed around the bacterium body. b: Images of bacteria that have yet to form capsules. Borrowed from [42].
Figure 5
Figure 5
a: Means by which the bacterial capsule will attenuate inflammation. b: Bacterially secreted proteases will attenuate immune response by degrading pro-inflammatory cytokines.
Figure 6
Figure 6
Schematic of signaling pathways involved in attenuating signaling pathways upon exposure to IL-10 (left) and IL-1ra (right)
Figure 7
Figure 7
Outline of applications of different immune evasive tactics from virology and bacteriology to biomaterials. a: Outline of inflammation when immune system is allowed to function unfettered. b: Possible viral design. Virally derived proteins like MT-7 can be released from a coating around the biomaterial to occupy chemokine binding domains and limit formation of a chemokine gradient. c: Possible bacterial design: By coating the material in an artificial derivative of a capsular polysaccharide, deposition of blood borne proteins will decrease, thereby limiting opsonization and inflammatory response. A similar approach would be coating the material in bacterially derived proteins that will inhibit complement deposition. d: A possible combination of viral and bacterial mechanisms. By coating the material in an artificial derivative of a capsular polysaccharide, the surface will become anti-biofouling. Additionally, the presence of viroreceptors will bind cytokines with high specificity, inhibiting the cytokine’s ability to bind to cellular receptors.
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