<i>Mycoplasma pneumoniae</i> and its role in asthma

Nisar, Nazima; Guleria, Randeep; Kumar, Sanjay; Chawla, T.C.; Biswas, Nihar Ranjan

doi:10.1136/pgmj.2006.049023

Cited by 68 publications

(56 citation statements)

References 40 publications

(41 reference statements)

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“…Interestingly, 44.4% of the patients suffered from asthma along with M. pneumoniae respiratory infection. Waites and Talkington and Nisar et al reported that M. pneumoniae infection may be related to asthma (10,20). Smoking is globally related with pulmonary diseases (21), but the results of this study did not show any significant rise in M. pneumoniae infection among cigarette smokers (P = 0.3).…”

Section: Discussioncontrasting

confidence: 55%

Epidemiology, clinical features, and laboratory detection of Mycoplasma pneumoniae infection in East Azerbaijan, Iran

Khanshour¹,

Conant²,

Juras³

et al. 2013

Turk J Med Sci

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Examining and measuring levels of suspended sediments of water column is a common application of close range remote sensing, because the technology offers an efficient and economical means of studying water quality problems. The aim of this experiment was to use close range remote sensing to determine the effect of increasing suspended sediment concentration containing different levels of organic matter on algal spectral patterns. The experiment was conducted in a small room with a 65-l volume water container. A Spectron Engineering SE-590 spectroradiometer with a 15 • optic was used to take the radiant measurements. The results indicate that the suspended sediment causes increasing spectral response in surface waters. The organic matter content of the suspended sediment has an effect on the spectral reflectance. Therefore, the organic content of the soil present in the water body can be estimated and this property of sediment can help us to recognize the sediment type present in the various layers of the water.

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Section: Discussioncontrasting

confidence: 55%

Epidemiology, clinical features, and laboratory detection of Mycoplasma pneumoniae infection in East Azerbaijan, Iran

Khanshour¹,

Conant²,

Juras³

et al. 2013

Turk J Med Sci

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“…However, we also observed a significant increase in eosinophilic infiltration in BALF samples from P-130-vaccinated and challenged mice (one animal from this group had 64% eosinophils in the differential leukocyte count). Such eosinophilia resembles that found in allergic asthma, consistent with reports that M. pneumoniae exacerbates atopy in asthmatic patients (reviewed by Nisar et al (30). Unfortunately, few reports have studied the influx of eosinophils during M. pneumoniae infection (particularly in acute models of infection), but Chu et al (6) found no evidence of eosinophils in rechallenged BALB/c mice 3 days postinfection (which also exhibited exacerbated disease).…”

Section: Discussionsupporting

confidence: 65%

Vaccination of BALB/c Mice with an Avirulent Mycoplasma pneumoniae P30 Mutant Results in Disease Exacerbation upon Challenge with a Virulent Strain

et al. 2012

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Mycoplasma pneumoniae is a significant human respiratory pathogen that causes high morbidity worldwide. No vaccine to prevent M. pneumoniae infection currently exists, since the mechanisms of pathogenesis are poorly understood. To this end, we constructed a P30 cytadhesin mutant (P-130) with a drastically reduced capacity for binding to erythrocytes and an inability to glide on glass substrates. This mutant was determined to be avirulent and cannot survive in the lungs of BALB/c mice. We also ascertained that the previously identified P30 gliding motility mutant II-3R is avirulent and also cannot be recovered from the lungs of mice after infection. Mutant P130 was then assessed for its efficacy as a live attenuated vaccine candidate in mice after challenge with wild-type M. pneumoniae. After vaccination with the P-130 P30 mutant, mice showed evidence of exacerbated disease upon subsequent challenge with the wild-type strain PI1428, which appears to be driven by a Th17 response and corresponding eosinophilia. Our results are in accordance with other reports of vaccine-induced disease exacerbation in rodents and emphasize the need to better understand the basic mechanisms of M. pneumoniae pathogenesis. Mycoplasma pneumoniae is a chronic human pathogen and the etiological agent of many cases of bronchitis and community-acquired pneumonia. Infection with this bacterium can also cause and/or exacerbate other diseases including asthma, myocarditis, sickle cell disease, and encephalitis. Outbreaks are common at such institutions as military bases, schools, and hospitals, where individuals are in close contact for long periods of time, reflecting the community-acquired nature of infections. Diagnosis is difficult as most medical laboratories do not screen for this pathogen, since quick and inexpensive tests are not readily available. Common first-line ␤-lactam antibiotics are ineffective treatments since mycoplasmas lack a cell wall; consequently, this pathogen is often overlooked during diagnosis of affected individuals, and common treatments do not target the source of the disease. This results in considerable economic and societal hardships due to lost and ineffective work/school time, making this pathogen a burden to public health (1, 42).Several virulence determinants of M. pneumoniae have been previously identified and characterized. This bacterium is thought primarily to exploit an extracellular niche and requires a complex tip structure to attach to its host's mucosal epithelium. The tip structure is also involved in gliding motility and cell division. Densely clustered on the surface of the tip structure are the major cytadhesins P1 and P30 and cytadherence-accessory proteins B/C, which are supported by a framework of interdependent cytoskeletal proteins, including HMW1, HMW2, HMW3, P200, P65, P41, and P24 (reviewed in reference 2). Cytadhesin protein P30 has been shown to be critical for both attachment (11, 32) and gliding motility, although its requirements for each are distinguishable (18). Thus, mutant II-...

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“…Although M. pneumoniae is a well established cause of asthma exacerbations, more recent data have suggested that it may also contribute to the pathogenesis of asthma (7)(8)(9)(10)(11)(12). The lipoprotein constituents of M. pneumoniae membrane play a critical role in immune recognition by the host and induction of the inflammatory response (13,14).…”

mentioning

confidence: 99%

Pulmonary Surfactant Phosphatidylglycerol Inhibits Mycoplasma pneumoniae-stimulated Eicosanoid Production from Human and Mouse Macrophages

Kandasamy¹,

Zarini

Chan³

et al. 2011

Journal of Biological Chemistry

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Mycoplasma pneumoniae is a human pathogen causing respiratory infections that are also associated with serious exacerbations of chronic lung diseases. Membranes and lipoproteins from M. pneumoniae induced a 4-fold increase in arachidonic acid (AA) release from RAW264.7 and a 2-fold increase in AA release from primary human alveolar macrophages. The bacterial lipoprotein mimic and TLR2/1 agonist Pam3Cys and the TLR2/6 agonist MALP-2 produced effects similar to those elicited by M. pneumoniae in macrophages by inducing the phosphorylation of p38 MAPK and p44/42 ERK1/2 MAP kinases and cyclooxygenase-2 (COX-2) expression. M. pneumoniae induced the generation of prostaglandins PGD 2 and PGE 2 from RAW264.7 cells and thromboxane B 2 (TXB 2 ) from human alveolar macrophages. Anti-TLR2 antibody completely abolished M. pneumoniae-induced AA release and TNF␣ secretion from RAW264.7 cells and human alveolar macrophages. Disruption of the phosphorylation of p44/ 42 ERK1/2 or inactivation of cytosolic phospholipase A 2 ␣ (cPLA 2 ␣) completely inhibited M. pneumoniae-induced AA release from macrophages. The minor pulmonary surfactant phospholipid, palmitoyl-oleoyl-phosphatidylglycerol (POPG), antagonized the proinflammatory actions of M. pneumoniae, Pam3Cys, and MALP-2 by reducing the production of AA metabolites from macrophages. The effect of POPG was specific, insofar as saturated PG, and saturated and unsaturated phosphatidylcholines did not have significant effect on M. pneumoniae-induced AA release. Collectively, these data demonstrate that M. pneumoniae stimulates the production of eicosanoids from macrophages through TLR2, and POPG suppresses this pathogen-induced response.

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Mycoplasma pneumoniae and its role in asthma

Cited by 68 publications

References 40 publications

Epidemiology, clinical features, and laboratory detection of Mycoplasma pneumoniae infection in East Azerbaijan, Iran

Epidemiology, clinical features, and laboratory detection of Mycoplasma pneumoniae infection in East Azerbaijan, Iran

Vaccination of BALB/c Mice with an Avirulent Mycoplasma pneumoniae P30 Mutant Results in Disease Exacerbation upon Challenge with a Virulent Strain

Pulmonary Surfactant Phosphatidylglycerol Inhibits Mycoplasma pneumoniae-stimulated Eicosanoid Production from Human and Mouse Macrophages

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