Characterization of an Immunoglobulin Binding Protein (IbpM) From Mycoplasma pneumoniae

Abstract

Bacteria evolved many ways to invade, colonize and survive in the host tissue. Such complex infection strategies of other bacteria are not present in the cell-wall less Mycoplasmas. Due to their strongly reduced genomes, these bacteria have only a minimal metabolism. Mycoplasma pneumoniae is a pathogenic bacterium using its virulence repertoire very efficiently, infecting the human lung. M. pneumoniae can cause a variety of conditions including fever, inflammation, atypical pneumoniae, and even death. Due to its strongly reduced metabolism, M. pneumoniae is dependent on nutrients from the host and aims to persist as long as possible, resulting in chronic diseases. Mycoplasmas evolved strategies to subvert the host immune system which involve proteins fending off immunoglobulins (Igs). In this study, we investigated the role of MPN400 as the putative factor responsible for Ig-binding and host immune evasion. MPN400 is a cell-surface localized protein which binds strongly to human IgG, IgA, and IgM. We therefore named the protein MPN400 immunoglobulin binding protein of Mycoplasma (IbpM). A strain devoid of IbpM is slightly compromised in cytotoxicity. Taken together, our study indicates that M. pneumoniae uses a refined mechanism for immune evasion.

Beware of Mycoplasma Anti-immunoglobulin Strategies

“…A highly similar homolog was identified in the closely related species Mycoplasma pneumoniae . Encoded by MPN400 and termed IbpM, this protein was shown to be functionally identical to protein M by Blötz et al in 2020 ( 74 ). In addition, distant homologs have been predicted in Mycoplasma iowae , M. gallisepticum , M. penetrans , Mycoplasma tullyi , Mycoplasma imitans , and Mycoplasma pirum .…”

Mycoplasma pneumoniae Infections: Pathogenesis and Vaccine Development

“…Immunoglobin binding protein (IbpM) is a surface protein encoded by MPN400 that binds strongly to various immunoglobulins (IgM, IgG, and IgA) produced by the host [ 45 ]. Blötz et al demonstrated that IbpM was required by M. pneumoniae to produce cytotoxic effects in host cells and is thus regarded as a virulent factor [ 45 ].…”

“…Similar to P1, P30 is also an important immunogenic factor [ 130 ]. Mutant M. pneumoniae without the gene encoding P30 is noninfectious and unable to adhere to host cells [ 45 ], which suggests that P30 could potentially be an ideal candidate target for a clinical vaccine. Szczepanek et al created an avirulent P30 adhesin mutant for assessing its efficacy as a live-attenuated vaccine candidate in mice [ 112 ].…”

Infection strategies of mycoplasmas: Unraveling the panoply of virulence factors

“…mycoids also expresses the MIB and MIP homologous proteins, whereas M. hominis, U. urealyticum, U. parvum, and U. diversum contain the MIB-MIP-encoding genes, but whether these genes are involved in the degradation of IgG remains unknown [103]. In addition, some mycoplasmas, such as M. genitalium and M. pneumoniae, lack the MIB-MIP system, but they can express protein M and DUF31-annotated genes in cells and play a role similar to that of the MIB-MIP system [7,141]. The third mechanism of degrading Ig is the expression of cysteine proteases (CysP).…”