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Inflammation-inducing Factors of Mycoplasma pneumoniae.

Shimizu T - Front Microbiol (2016)

Bottom Line: Mycoplasma pneumoniae, which causes mycoplasmal pneumonia in human, mainly causes pneumonia in children, although it occasionally causes disease in infants and geriatrics.Lipoproteins induce inflammatory responses through Toll-like receptors (TLR) 2.TLR4 and autophagy are involved in this TLR2-independent inflammation.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Veterinary Public Health, Joint Faculty of Veterinary Medicine, Yamaguchi University Yamaguchi, Japan.

ABSTRACT
Mycoplasma pneumoniae, which causes mycoplasmal pneumonia in human, mainly causes pneumonia in children, although it occasionally causes disease in infants and geriatrics. Some pathogenic factors produced by M. pneumoniae, such as hydrogen peroxide and Community-Acquired Respiratory Distress Syndrome (CARDS) toxin have been well studied. However, these factors alone cannot explain this predilection. The low incidence rate of mycoplasmal pneumonia in infants and geriatrics implies that the strong inflammatory responses induced by M. pneumoniae coordinate with the pathogenic factors to induce pneumonia. However, M. pneumoniae lacks a cell wall and does not possess an inflammation-inducing endotoxin, such as lipopolysaccharide (LPS). In M. pneumoniae, lipoproteins were identified as an inflammation-inducing factor. Lipoproteins induce inflammatory responses through Toll-like receptors (TLR) 2. Because Mycoplasma species lack a cell wall and lipoproteins anchored in the membrane are exposed, lipoproteins and TLR2 have been thought to be important for the pathogenesis of M. pneumoniae. However, recent reports suggest that M. pneumoniae also induces inflammatory responses also in a TLR2-independent manner. TLR4 and autophagy are involved in this TLR2-independent inflammation. In addition, the CARDS toxin or M. pneumoniae cytadherence induces inflammatory responses through an intracellular receptor protein complex called the inflammasome. In this review, the inflammation-inducing factors of M. pneumoniae are summarized.

No MeSH data available.


Related in: MedlinePlus

Summary of the inflammation-inducing pathways in Mycoplasma pneumoniae infection. The following four pathways are involved in the induction of inflammatory responses: (1) recognition of lipoprotein by TLR2, (2) autophagy-mediated signaling, (3) activation of inflammasomes, and (4) cytadherence property.
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Figure 2: Summary of the inflammation-inducing pathways in Mycoplasma pneumoniae infection. The following four pathways are involved in the induction of inflammatory responses: (1) recognition of lipoprotein by TLR2, (2) autophagy-mediated signaling, (3) activation of inflammasomes, and (4) cytadherence property.

Mentions: In this review, the molecular mechanisms of inflammatory responses induced by M. pneumoniae were reviewed (Figure 2). The following four pathways are important for the induction of inflammatory responses in M. pneumoniae infection: 1) recognition of lipoprotein by TLR2, 2) autophagy-mediated signaling; 3) activation of inflammasomes, and 4) cytadherence property. Lipoproteins, which were the first immunostimulants discovered in Mycoplasma species, have been well studied. However, the structures of the lipoproteins in Mycoplasma species are identical to those of lipoproteins from other bacteria, including normal microflora. Therefore, lipoproteins alone are insufficient to explain the inflammatory responses induced by M. pneumoniae. M. pneumoniae also has the ability to induce inflammatory responses through a TLR2-independent pathway. Autophagy and TLR4 are involved in this induction. Some pro-inflammatory cytokines, such as IL-1β and IL-18, are matured and released through inflammasome activation. Inflammasome activation is necessary to release these cytokines during M. pneumoniae infection. It is noteworthy that CARDS toxin enhances inflammasome activation. The distribution of CARDS toxin in Mycoplasma species is limited to a small number of Mycoplasma species. In addition, cytadherent property of M. pneumoniae is strongly associated with the autophagy/TLR4- and inflammasome- mediated induction of inflammatory responses. Although some Mycoplasma species, such as M. genitalium and M. gallisepticum, have partially similar adhesin, cytadherence mediated by P1 adhesin is unique in M. pneumoniae. These characteristics may contribute to the greater ability of M. pneumoniae to induce inflammatory responses than non-pathogenic Mycoplasma species.


Inflammation-inducing Factors of Mycoplasma pneumoniae.

Shimizu T - Front Microbiol (2016)

Summary of the inflammation-inducing pathways in Mycoplasma pneumoniae infection. The following four pathways are involved in the induction of inflammatory responses: (1) recognition of lipoprotein by TLR2, (2) autophagy-mediated signaling, (3) activation of inflammasomes, and (4) cytadherence property.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4814563&req=5

Figure 2: Summary of the inflammation-inducing pathways in Mycoplasma pneumoniae infection. The following four pathways are involved in the induction of inflammatory responses: (1) recognition of lipoprotein by TLR2, (2) autophagy-mediated signaling, (3) activation of inflammasomes, and (4) cytadherence property.
Mentions: In this review, the molecular mechanisms of inflammatory responses induced by M. pneumoniae were reviewed (Figure 2). The following four pathways are important for the induction of inflammatory responses in M. pneumoniae infection: 1) recognition of lipoprotein by TLR2, 2) autophagy-mediated signaling; 3) activation of inflammasomes, and 4) cytadherence property. Lipoproteins, which were the first immunostimulants discovered in Mycoplasma species, have been well studied. However, the structures of the lipoproteins in Mycoplasma species are identical to those of lipoproteins from other bacteria, including normal microflora. Therefore, lipoproteins alone are insufficient to explain the inflammatory responses induced by M. pneumoniae. M. pneumoniae also has the ability to induce inflammatory responses through a TLR2-independent pathway. Autophagy and TLR4 are involved in this induction. Some pro-inflammatory cytokines, such as IL-1β and IL-18, are matured and released through inflammasome activation. Inflammasome activation is necessary to release these cytokines during M. pneumoniae infection. It is noteworthy that CARDS toxin enhances inflammasome activation. The distribution of CARDS toxin in Mycoplasma species is limited to a small number of Mycoplasma species. In addition, cytadherent property of M. pneumoniae is strongly associated with the autophagy/TLR4- and inflammasome- mediated induction of inflammatory responses. Although some Mycoplasma species, such as M. genitalium and M. gallisepticum, have partially similar adhesin, cytadherence mediated by P1 adhesin is unique in M. pneumoniae. These characteristics may contribute to the greater ability of M. pneumoniae to induce inflammatory responses than non-pathogenic Mycoplasma species.

Bottom Line: Mycoplasma pneumoniae, which causes mycoplasmal pneumonia in human, mainly causes pneumonia in children, although it occasionally causes disease in infants and geriatrics.Lipoproteins induce inflammatory responses through Toll-like receptors (TLR) 2.TLR4 and autophagy are involved in this TLR2-independent inflammation.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Veterinary Public Health, Joint Faculty of Veterinary Medicine, Yamaguchi University Yamaguchi, Japan.

ABSTRACT
Mycoplasma pneumoniae, which causes mycoplasmal pneumonia in human, mainly causes pneumonia in children, although it occasionally causes disease in infants and geriatrics. Some pathogenic factors produced by M. pneumoniae, such as hydrogen peroxide and Community-Acquired Respiratory Distress Syndrome (CARDS) toxin have been well studied. However, these factors alone cannot explain this predilection. The low incidence rate of mycoplasmal pneumonia in infants and geriatrics implies that the strong inflammatory responses induced by M. pneumoniae coordinate with the pathogenic factors to induce pneumonia. However, M. pneumoniae lacks a cell wall and does not possess an inflammation-inducing endotoxin, such as lipopolysaccharide (LPS). In M. pneumoniae, lipoproteins were identified as an inflammation-inducing factor. Lipoproteins induce inflammatory responses through Toll-like receptors (TLR) 2. Because Mycoplasma species lack a cell wall and lipoproteins anchored in the membrane are exposed, lipoproteins and TLR2 have been thought to be important for the pathogenesis of M. pneumoniae. However, recent reports suggest that M. pneumoniae also induces inflammatory responses also in a TLR2-independent manner. TLR4 and autophagy are involved in this TLR2-independent inflammation. In addition, the CARDS toxin or M. pneumoniae cytadherence induces inflammatory responses through an intracellular receptor protein complex called the inflammasome. In this review, the inflammation-inducing factors of M. pneumoniae are summarized.

No MeSH data available.


Related in: MedlinePlus