Abstract

ABSTRACTMycoplasmas are small, genome-reduced bacteria. They are obligate parasites that can be found in a wide range of host species, including the majority of livestock animals and humans. Colonization of the host can result in a wide spectrum of outcomes. In many cases, these successful parasites are considered commensal, as they are found in the microbiota of asymptomatic carriers. Conversely, mycoplasmas can also be pathogenic, as they are associated with a range of both acute and chronic inflammatory diseases which are problematic in veterinary and human medicine. The chronicity of mycoplasma infections and the ability of these bacteria to infect even recently vaccinated individuals clearly indicate that they are able to successfully evade their host’s humoral immune response. Over the years, multiple strategies of immune evasion have been identified in mycoplasmas, with a number of them aimed at generating important antigenic diversity. More recently, mycoplasma-specific anti-immunoglobulin strategies have also been characterized. Through the expression of the immunoglobulin-binding proteins protein M or mycoplasma immunoglobulin binding (MIB), mycoplasmas have the ability to target the host’s antibodies and to prevent them from interacting with their cognate antigens. In this review, we discuss how these discoveries shed new light on the relationship between mycoplasmas and their host’s immune system. We also propose that these strategies should be taken into consideration for future studies, as they are key to our understanding of mycoplasma diseases' chronic and inflammatory nature and are probably a contributing factor to reduce vaccine efficacy.

Highlights

  • The classes and subclasses of pathogen-specific immunoglobulins should be systematically titrated, as they can be targeted in a differential manner by bacterial effectors and their involvement in the immune response has been shown to vary over the course of long infections

  • It seems that they have evolved elaborate and independent strategies to cope with the selective pressure applied by their hosts’ immune systems, making the most of their quasiminimal genetic information

  • Since the 1980s, mycoplasmologists have documented the mechanisms leading to an ever-changing surface antigenic structure of mycoplasma cells

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Summary

Introduction

Most studies report that vaccination yields a typical immune response with high titers of circulating specific antibodies, followed by an often disappointing level of protection when vaccinated individuals are challenged with pathogenic strains [26,27,28,29]. Of particular interest is the ability of mycoplasmas to successfully thwart their host’s humoral immune response, as these bacteria can infect recently vaccinated individuals and persist even in the presence of high titers of specific antibodies [21, 22, 33]. In addition to antibody degradation by proteolysis, strategies based on immunoglobulin-binding proteins (IBP) have been discovered in mycoplasmas.

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