This is from 2005 but interesting. The authors reference previous research
showing that macrophages infected with M. avium produce less Tumor
Necrosis Factor-alpha and inducible Nitric Oxide Synthase compared with
cells infected by M. smegmatis which is usually non-pathogenic. These
substances are part of the normal immune response to infections and other
stressors. A reduced immune response to infection fits with the recent
discovery that paratuberculosis prevents macrophages from killing E. coli,
but it seems to me that it also suggests that the immune insufficiency or
deficiency might extend beyond E. coli to allow other opportunistic
infections.

-- Dale
<http://DaleRoose.com/>
When John McCain begins a sentence with "Everybody knows" or "It's common
knowledge" or "It's been reported everywhere in the media", whatever
follows should be questioned.
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<http://lib.bioinfo.pl/meid:22798>

Infect Immun. 2005 Oct ;73:6499-507 16177323 (P,S,E,B)

Activation and mitogen-activated protein kinase regulation of
transcription factors Ets and NF-kappaB in Mycobacterium-infected
macrophages and role of these factors in tumor necrosis factor alpha and
nitric oxide synthase 2 promoter function.

Seong-Beom Lee, Jeffrey S Schorey

Previous studies have shown that primary murine macrophages infected with
Mycobacterium avium produced lower levels of tumor necrosis factor alpha
(TNF-alpha) and inducible nitric oxide synthase 2 (NOS2) compared to cells
infected with nonpathogenic Mycobacterium smegmatis. TNF-alpha and NOS2
levels correlated with and were dependent on the activation of
mitogen-activated protein kinases (MAPKs) p38 and extracellular
signal-regulated kinase 1/2 (ERK1/2). To define the macrophage
transcriptional responses dependent on ERK1/2 activation following a
mycobacterial infection, we used RAW 264.7 cells transfected with a
TNF-alpha or NOS2 promoter vector. We determined that macrophages infected
with M. avium compared to M. smegmatis showed diminished TNF-alpha and
NOS2 promoter activity. A more pronounced difference in promoter activity
was observed when only the consensus ETS and NF-kappaB binding sites were
used as promoters. Mutational analysis of the ETS and NF-kappaB binding
sites present on the TNF-alpha and NOS2 promoters, respectively, showed
that these sites were essential for a functional promoter. Moreover, the
Ets/Elk but not the NF-kappaB transcriptional response was dependent on
ERK1/2. This correlated with the requirement for ERK1/2 in TNF-alpha but
not NOS2 promoter activity. Our data indicate that the increased Ets/Elk
and NF-kappaB promoter activities associated with M. smegmatis-infected
macrophages are responsible, at least in part, for the increased TNF-alpha
and NOS2 production observed in these infected cells and that ERK1/2 is
required for Ets/Elk activity and full TNF-alpha production.