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1  lung disease developed after infection with M. pulmonis.
2 amide (CYP) and inoculated with 10(7) CFU of M. pulmonis.
3 e could demonstrate that it was expressed in M. pulmonis.
4 ious Bcg and H-2 genotypes for resistance to M. pulmonis.
5 hmatic airways to facilitate colonization by M. pulmonis and the capacity of M. pulmonis to exacerbat
6 erior to single PCR or culture for detecting M. pulmonis, and that M. pulmonis is present in all but
7       Both Tn4001C and Tn4001T transposed in M. pulmonis, and Tn4001T transposed in M. arthritidis.
8   Rats were inoculated with 3 X 10(7) CFU of M. pulmonis at 10 days prior to breeding (-10) or at ges
9  model clearly provides a mechanism by which M. pulmonis can alter its surface architecture and also
10                               Populations of M. pulmonis cells that arose during growth in different
11                                          The M. pulmonis chromosome has two hsd loci, both of which c
12  not be cultured and identified 2 additional M. pulmonis-contaminated CAR bacillus isolates.
13  of 61 (34%) CAR bacillus samples from which M. pulmonis could not be cultured and identified 2 addit
14 nificant role in determining the severity of M. pulmonis disease.
15                      Mice were infected with M. pulmonis for measurements of alveolar fluid clearance
16 tsZ gene was overexpressed, and the purified M. pulmonis FtsZ bound GTP.
17                            Expression of the M. pulmonis ftsZ gene in E. coli inhibited cell division
18                                          The M. pulmonis ftsZ gene was overexpressed, and the purifie
19  We report here that a single recombinase in M. pulmonis, HvsR, catalyses independent DNA inversions
20                     Nested PCR also detected M. pulmonis in 14 of 20 (70%) paraffin sections of lung
21                     Nested PCR also detected M. pulmonis in 21 of 61 (34%) CAR bacillus samples from
22 licated as a virulence determining factor in M. pulmonis-induced murine respiratory disease, the prec
23 ary clearance and altered airway function in M. pulmonis-infected animals.
24                          CYP pretreatment of M. pulmonis-infected iNOS(+/+) and iNOS(-/-) mice reduce
25 e changes in blood vessels and lymphatics in M. pulmonis-infected mice.
26           Ang1 and Ang2 protein increased in M. pulmonis-infected mouse airways but came from differe
27 rce for capillary remodeling into venules in M. pulmonis-infected mouse airways.
28 n of venous markers, and leukocyte influx in M. pulmonis-infected mouse airways.
29                                              M. pulmonis-infected MTEs, but not those infected with a
30 r, AX102 exaggerated leakage at 7 days after M. pulmonis infection and increased vascular remodeling
31  lymphangiogenesis in inflamed airways after M. pulmonis infection because expression of the integrin
32 clude that the polarized stimulus created by M. pulmonis infection differentially changes the size, s
33 t in mice genetically predisposed to asthma, M. pulmonis infection elicits an inflammatory milieu in
34  a significant impact on lung disease due to M. pulmonis infection in mice.
35 ymphangiogenesis occurs in mouse lungs after M. pulmonis infection through a mechanism involving sign
36                                   Similar to M. pulmonis infection, systemic overexpression of angiop
37 g and the consequences of inflammation after M. pulmonis infection.
38 A were present in EphA2-deficient mice after M. pulmonis infection.
39  culture for detecting M. pulmonis, and that M. pulmonis is present in all but four CAR bacillus isol
40 infected with 10(10) colony-forming units of M. pulmonis, killed mycoplasmas within 6 h.
41 nduced both humoral and cellular immunity to M. pulmonis, largely prevented infection (vaccination),
42 nst two MnuA peptide sequences identified an M. pulmonis membrane protein of approximately 42 kDa by
43                     Further study of the MTE-M. pulmonis model should elucidate the molecular mechani
44               Of 27 samples known to contain M. pulmonis, only 12 (44%) were positive in the first PC
45 anasal infection with 5 x 10(4) CFU virulent M. pulmonis organisms.
46 that when encased within a biofilm, cells of M. pulmonis producing a short form of the Vsa protein we
47                                              M. pulmonis producing a VsaA protein with about 40 tande
48          Sequencing of the ftsZ homolog from M. pulmonis revealed that it was highly homologous to ot
49                         The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented ex
50                     We isolated and analyzed M. pulmonis strain CT variants (CT182 and derivatives) t
51 s comprising a 10-kb region of the genome of M. pulmonis strain KD735-15.
52                                         When M. pulmonis strain X1048 was propagated in laboratory cu
53 oculated with an avirulent, poorly infective M. pulmonis strain, 14 (19%) were positive by nested PCR
54                                              M. pulmonis strains that produce VsaA with about 40 tand
55                    Isolation and analysis of M. pulmonis strains that produced Vsa proteins other tha
56                             In contrast, the M. pulmonis strains that produced VsaA R40 were highly r
57 ate the Vsa proteins nonspecifically mediate M. pulmonis surface interactions and function to sterica
58          To examine vsa genes in a strain of M. pulmonis that is unrelated to KD735-15, strain CT was
59 fected by the bacterium Mycoplasma pulmonis (M. pulmonis), the segment of the microvasculature that s
60                  Furthermore, the ability of M. pulmonis to alter transport without killing the host
61 onization by M. pulmonis and the capacity of M. pulmonis to exacerbate symptoms associated with acute
62 ough release of IFN-gamma and the ability of M. pulmonis to trigger the production of Th2-type cytoki
63 re inoculated intranasally with 10(4) CFU of M. pulmonis UAB CT and evaluated at 21 days postinfectio
64 nd characterized genes encoding V-1 from two M. pulmonis UAB CT V-1 variants that differ in hemadsorp
65 were infected intranasally with 10(5) CFU of M. pulmonis UAB CT, and their lungs were quantitatively
66            To determine the direct effect of M. pulmonis upon transepithelial ion transport in the ab
67                                 Furthermore, M. pulmonis Vsa variants were susceptible to the polypep
68                                              M. pulmonis was isolated from the placenta, amniotic flu
69                     Altered transport due to M. pulmonis was not merely a result of epithelial cell d
70       The dispensable and essential genes of M. pulmonis were compared with those reported for Mycopl
71  with CAR bacillus isolates known to contain M. pulmonis, whereas single PCR gave no positive results
72         In the absence of AMs, incubation of M. pulmonis with the peroxynitrite generator 3-morpholin

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