Native Mycoplasma Pneumoniae P1 Antigen

Hosts are typically coinfected by multiple parasite species whose interactions might be synergetic or antagonistic, producing unpredictable physiological and pathological impacts on the host. This study shows the interaction betweenPlasmodiumspp. andLeucocytozoonspp. in birds experimentally infected or not infected withMycoplasma gallisepticum. In 1994, the bacteriumMycoplasma gallisepticumjumped from poultry to wild birds in which it caused a major epidemic in North America. Birds infected withM. gallisepticumshow conjunctivitis as well as increased levels of corticosterone. Malaria and other haemosporidia are widespread in birds, and chronic infections become apparent with the detectable presence of the parasite in peripheral blood in response to elevated levels of natural or experimental corticosterone levels. Knowing the immunosuppressive effect of corticosterone on the avian immune system, we tested the hypothesis that chronic infections ofPlasmodiumspp. andLeucocytozoonspp. in house finches would respond to experimental inoculation withM. gallisepticumas corticosterone levels are known to increase following inoculation. Plasmodiumspp. infection intensity increased within days ofM. gallisepticuminoculation as shown both by the appearance of infected erythrocytes and by the increase in the number and the intensity of positive PCR tests. Leucocytozoonspp. infection intensity increased whenPlasmodiumspp. infection intensity increased, but not in response toM. gallisepticuminoculation.Leucocytozoonspp. andPlasmodiumspp. seemed to compete in the host as shown by a negative correlation between the changes in their PCR score when both pathogens were present in the same individual. Host responses to coinfection with multiple pathogens measured by the hematocrit and white blood cell count depended on the haemosporidian community composition. Host investment in the leukocyte response was higher in the single-haemosporidia-infected groups when birds were infected withM. gallisepticum. A trade-off was observed between the immune control of the chronic infection (Plasmodiumspp./Leucocytozoonspp.) and the immune response to the novel bacterial infection (M. gallisepticum).

Azithromycin is considered an effective drug to treat the perinatal mycoplasma infection. However, there is a lack of studies on developmental toxicity of azithromycin. In this study, we observed the developmental toxicity of fetal liver induced by prenatal azithromycin exposure (PAE) in mice and explored the potential mechanism. Pregnant Kunming mice were intraperitoneally injected with azithromycin (37.5 and 150 mg/kg.d) from gestational day (GD) 9 to 18. After PAE, the bodyweight gain rates of pregnant mice and the birthweights of the offspring were decreased, and the liver morphology, development indexes and metabolic function were all altered in different degree in the PAE fetuses. Meanwhile, PAE decreased the fetal serum insulin-like growth factor 1 (IGF1) levels and liver IGF1 signal pathway expression, accompanied by glucocorticoid receptor-CCAAT enhancer-binding protein alpha (GR-C/EBP alpha) signal enhancement. Furthermore, azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBP alpha signal and reducing the expression and secretion levels of IGF1 in HepG2 cells. These changes could be reversed by GR siRNA or exogenous IGF1. These results indicated that PAE could cause fetal liver developmental toxicity in mice, and one of the main mechanisms was that azithromycin activated the GR-C/EBP alpha signal, inhibited the IGF1 signal pathway, and then disturbed the hepatic proliferation, apoptosis, differentiation, and glycose and lipid metabolism.