ライフサイエンスコーパス: M. hyopneumoniae

1 ng infection, our analysis indicated that 79 M. hyopneumoniae genes were differentially expressed (P

2 an Escherichia coli opal suppressor host and M. hyopneumoniae bound specifically to swine cilia, and

3 evealed that pigs infected with both SIV and M. hyopneumoniae coughed significantly more than pigs in

4 howing that P102 is expressed in vivo during M. hyopneumoniae infections.

5 How M. hyopneumoniae responds to changing environments in th

6 Thus, it is not clear how M. hyopneumoniae evades the immune response and establis

7 Most importantly, M. hyopneumoniae-infected pigs with minimal to nondetect

8 ting that a processing event had occurred in M. hyopneumoniae.

9 c lesions were more severe and persistent in M. hyopneumoniae-infected pigs.

10 At 28 or 38 days after PRRSV inoculation, M. hyopneumoniae-infected pigs still exhibited lesions t

11 Unlike other mycoplasmas, M. hyopneumoniae contains few genes with tandem repeat s

12 In contrast, nonpathogenic M. hyopneumoniae and M. flocculare at concentrations of

13 enic Mycoplasma hyopneumoniae, nonpathogenic M. hyopneumoniae, and Mycoplasma flocculare on intracell

14 disease process is initiated by adherence of M. hyopneumoniae to the cilia of swine respiratory epith

15 Numerous PCR assays for the detection of M. hyopneumoniae have been developed, targeting several

16 hospholipase C, also abolished the effect of M. hyopneumoniae.

17 ing of 632 of the 698 open reading frames of M. hyopneumoniae was constructed and used to study gene

18 In this study, a panel of isolates of M. hyopneumoniae, M. flocculare, M. hyorhinis, and M. hy

19 assays tested did not detect all isolates of M. hyopneumoniae.

20 urther delineate the molecular mechanisms of M. hyopneumoniae interactions with ciliated epithelium,

21 M. hyosynoviae were tested with a number of M. hyopneumoniae-specific PCR assays.

22 ay serve as a signal for the pathogenesis of M. hyopneumoniae.

23 A comparison of the R1 regions of M. hyopneumoniae strains displaying variation in cilium

24 infection did not influence the severity of M. hyopneumoniae infection, although microscopic lesions

25 Recently, genetic diversity among strains of M. hyopneumoniae was demonstrated.

26 e P97 cilium adhesin in different strains of M. hyopneumoniae, but the extent of genetic variation am

27 ion, although microscopic lesions typical of M. hyopneumoniae were more severe in PRRSV-infected pigs

28 In Ca2+-free medium, pathogenic M. hyopneumoniae still increased [Ca2+]i in tracheal cel

29 l within 100 s of the addition of pathogenic M. hyopneumoniae strain 91-3 (300 microg/ml), and this i

30 These results suggest that pathogenic M. hyopneumoniae activates receptors that are coupled to

31 Since M. hyopneumoniae is a worldwide problem, it is reasonabl

32 Some M. hyopneumoniae PCR assays tested did not detect all is

33 is does not exist, although it is clear that M. hyopneumoniae adheres to porcine ciliated epithelium

34 Previous studies demonstrated that M. hyopneumoniae, which produces a chronic bronchopneumo

35 These results indicate that M. hyopneumoniae infection potentiates PRRSV-induced dis

36 ing gene was present as a single copy in the M. hyopneumoniae chromosome.

37 ermutation test identified a location in the M. hyopneumoniae genome where there is spatial clusterin

38 ups, with minimal levels of pneumonia in the M. hyopneumoniae-only-infected pigs.

39 specific and capable of detecting all of the M. hyopneumoniae isolates used in this study were develo

40 rsity on the accuracy and sensitivity of the M. hyopneumoniae PCR assays could result in false-negati

41 ual-infected pigs was similar to that of the M. hyopneumoniae-only-infected group, and the pneumonia

42 potentiation found with dual infection with M. hyopneumoniae and PRRSV.

43 In this study, pigs were inoculated with M. hyopneumoniae 21 days prior to inoculation with SIV.

44 Pigs were inoculated with M. hyopneumoniae 21 days prior to, simultaneously with,