Expression of interleukin-10 and suppressor of cytokine signaling-3 associated with susceptibility of cattle to infection with Mycobacterium avium subsp paratuberculosis.
OBJECTIVE
To determine functional characteristics of monocytes obtained from cows with subclinical infection with Mycobacterium avium subsp paratuberculosis (MAP) that may have predisposed those cows to becoming infected with MAP SAMPLE POPULATION: Monocytes obtained from 5 uninfected cows and 5 cows subclinically infected with MAP in a herd with a high prevalence of paratuberculosis (ie, Johne's disease).


METHODS
Monocytes from uninfected and subclinically infected cows were incubated with MAP for 2, 6, 24, 72, or 96 hours. Variables measured included expression of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-10, IL-12, transforming growth factor-beta, and suppressor of cytokine signaling-3 (SOCS-3); apoptosis of monocytes; acidification of phagosomes; and killing of MAP.


RESULTS
Monocytes from infected cows had greater expression of IL-10 and SOCS-3 at 2 hours of coincubation with MAP and lower expression of TNF-alpha and IL-12 when results for all incubation times were combined. Monocytes from infected cows had a greater capacity to acidify phagosomes. No differences were observed in the rate of apoptosis or capacity of monocytes to kill MAP organisms.


CONCLUSIONS
Monocytes obtained from cows with subclinical infection with MAP had upregulated expression of IL-10 and SOCS-3 within the first 2 hours after exposure to MAP organisms. Although this did not inhibit acidification of phagosomes, apoptosis of monocytes, or attenuation of the capacity to kill MAP organisms, it may have attenuated the capacity of mononuclear phagocytes to initiate inflammatory and adaptive immune responses.
Weiss
Douglas J
DJ
Department of Veterinary PathoBiology, College of Veterinary Medicine, University of Minnesota, Saint Paul, MN 55108, USA.
Evanson
Oral A
OA
Souza
Cleverson D
CD
D000818:Animals; D002417:Cattle; D002418:Cattle Diseases / Q000235:genetics* / Q000276:immunology*; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D005786:Gene Expression Regulation; D020022:Genetic Predisposition to Disease; D016753:Interleukin-10 / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D008262:Macrophage Activation; D009000:Monocytes / Q000502:physiology; D010283:Paratuberculosis / Q000235:genetics* / Q000276:immunology*; D010588:Phagosomes / Q000502:physiology; D012097:Repressor Proteins / Q000096:biosynthesis; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D016207:Cytokines; D012097:Repressor Proteins; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12