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1 cally infected with the respiratory pathogen Mycoplasma pulmonis.
2 virulence of the murine respiratory pathogen Mycoplasma pulmonis.
3 were undertaken to examine gene transfer in Mycoplasma pulmonis.
4 /lpr, and B6-gld/gld mice were infected with Mycoplasma pulmonis.
5 iable R-M systems encoded by the hsd loci of Mycoplasma pulmonis.
6 lyze one of the membrane nuclease genes from Mycoplasma pulmonis.
7 with 10(5) or 10(7) colony-forming units of Mycoplasma pulmonis.
8 esponse in the airways of mice infected with Mycoplasma pulmonis.
9 were immunized i.m. with DNA for one or two Mycoplasma pulmonis Ags (A7-1, A8-1) beginning either 1
10 (a) chronic respiratory tract infection with Mycoplasma pulmonis and (b) adenoviral transduction of a
11 e ftsZ is present in two mycoplasma species, Mycoplasma pulmonis and Acholeplasma laidlawii, which ar
12 d (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection
14 attempts to introduce transposon Tn4001 into Mycoplasma pulmonis and Mycoplasma arthritidis have not
15 etic analysis, TraE homologs of S. kunkelii, Mycoplasma pulmonis and Mycoplasma fermentans cluster to
16 d configuration in Mycoplasma pneumoniae and Mycoplasma pulmonis, and in both the d and l configurati
17 nasal or nasal-pulmonary immunizations with Mycoplasma pulmonis antigen alone or with cholera toxin
18 ens (Vsa) of the murine respiratory pathogen Mycoplasma pulmonis are associated with the virulence of
21 ovokes histamine release, we exposed mice to Mycoplasma pulmonis, comparing responses in wild-type an
24 synthase(-/-) (iNOS(-/-)) mice infected with Mycoplasma pulmonis developed higher bacterial numbers a
25 of AM depletion on intrapulmonary killing of Mycoplasma pulmonis during the early phase of infection
29 Airways of LTbeta(-/-) mice infected with Mycoplasma pulmonis had significantly more lymphangiogen
30 addition to phase-variable surface proteins, Mycoplasma pulmonis has a family of phase-variable restr
31 Although the variation of V-1 antigens of Mycoplasma pulmonis has been correlated with variable ex
32 e tandem repeat region of the Vsa protein of Mycoplasma pulmonis has previously been shown to modulat
34 ty and reversibility of vessel remodeling in Mycoplasma pulmonis-infected mice using immunohistochemi
35 remodeling in the respiratory tract by using Mycoplasma pulmonis infection as a model of sustained in
38 ideal opportunity to study this process, as Mycoplasma pulmonis infection of mouse airways induces w
39 l of chronic airway inflammation produced by Mycoplasma pulmonis infection of the airways of mice or
40 in airway lymphatics at 14 and 28 days after Mycoplasma pulmonis infection of the respiratory tract.
41 t mice whose airways were inflamed by either Mycoplasma pulmonis infection or ovalbumin sensitization
42 use strains differ markedly in resistance to Mycoplasma pulmonis infection, and investigation of thes
43 rine respiratory mycoplasmosis (MRM), due to Mycoplasma pulmonis infection, is an excellent animal mo
44 r baseline conditions and 3 to 28 days after Mycoplasma pulmonis infection, using prospero heomeobox
45 f sustained airway inflammation in mice with Mycoplasma pulmonis infection, which is known to be acco
49 flammation in mice infected by the bacterium Mycoplasma pulmonis (M. pulmonis), the segment of the mi
51 uman synovial sections and sections from the Mycoplasma pulmonis MRL-lpr/lpr mouse arthritis model.
53 7-day infection by the respiratory pathogen Mycoplasma pulmonis, or iv) leakage after bradykinin cha
55 al and bronchial epithelial cell surfaces by Mycoplasma pulmonis, submucosal and intraluminal immune
56 way inflammation, produced by infection with Mycoplasma pulmonis, was compared in strains of mice kno
57 el of asthma and the natural murine pathogen Mycoplasma pulmonis, we provide a mechanistic explanatio
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