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Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza.

Kapczynski DR, Liljebjelke K, Kulkarni G, Hunt H, Jiang HJ, Petkov D - BMC Proc (2011)

Bottom Line: Cellular immunity was determined by cytotoxic lysis of B2/B2 infected lung target cells and proliferation of T cells following exposure to LPAI.Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds.T cell proliferation was determined to be highest when exposed to the homologous virus.

View Article: PubMed Central - HTML - PubMed

Affiliation: Southeast Poultry Research Laboratory, Agricultural Research Service, USA, Department of Agriculture, 934 College Station Road, Athens, GA 30605, USA. darrell.kapczynski@ars.usda.gov.

ABSTRACT

Background: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little is known about cellular immunity following a primary AI infection in poultry, especially regarding cytotoxic T lymphocytes (CTL's).

Methods: In these studies, major histocompatibility complex (MHC)-defined (B2/B2) chickens were infected with low pathogenic AI (LPAI) H9N2 and clinical signs of disease were monitored over a two weeks period. Splenic lymphocytes from infected and naïve birds were examined for cross reactivity against homologous and heterologous (H7N2) LPAI by ex vivo stimulation. Cellular immunity was determined by cytotoxic lysis of B2/B2 infected lung target cells and proliferation of T cells following exposure to LPAI.

Results: Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds. Splenic lymphocytes derived from H9N2-infected birds displayed lysis of both homologous (H9N2) and heterologous (H7N2) infected target cells, whereas lymphocytes obtained from sham-infected birds did not. T cell proliferation was determined to be highest when exposed to the homologous virus.

Conclusions: Taken together these data extend the findings that cellular immunity, including CTL's, is cross reactive against heterologous isolates of AI and contribute to protection following infection.

No MeSH data available.


Related in: MedlinePlus

Recognition of homologous and heterologous LPAI ex vivo by splenocytes derived from H9N2-infected chickens. The cross-reactivity of lymphocytes was tested with MHC- matched B2/B2 lung cell cultures infected with H9N2 or H7N2 LPAI. Effector:target (E:T) ratios were 10, 20 and 40 for all subjects. Standard deviation of the means was <10%. Spontaneous lysis from splenocytes derived from naive birds were <7 % against either virus (data not shown).
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Figure 2: Recognition of homologous and heterologous LPAI ex vivo by splenocytes derived from H9N2-infected chickens. The cross-reactivity of lymphocytes was tested with MHC- matched B2/B2 lung cell cultures infected with H9N2 or H7N2 LPAI. Effector:target (E:T) ratios were 10, 20 and 40 for all subjects. Standard deviation of the means was <10%. Spontaneous lysis from splenocytes derived from naive birds were <7 % against either virus (data not shown).

Mentions: Splenic T cells from inbred chickens infected with H9N2 AI lysed target cells infected with either homologous or H7N2 AI at all effector:target (E:T) ratios tested (Fig 2). A dose response based on E:T ratios was observed. At E:T ratio of 40:1, 52 % of H9N2-infected B2/B2 lung target cells were lysed, while 43 % of H7N2-infected target cells were lysed. At lower E:T ratios, approximately 18 % (20:1) and 10 % (10:1) of infected target cells were lysed in either H9N2 or H7N2-infected lung cells. The splenic T cells from H9N2 infected birds did not lyse uninfected target cells, although spontaneous lysis was approximately 7 % (data not shown). In addition, lymphocytes obtained from sham-infected birds did not lyse infected or control lung cell cultures (data not shown).


Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza.

Kapczynski DR, Liljebjelke K, Kulkarni G, Hunt H, Jiang HJ, Petkov D - BMC Proc (2011)

Recognition of homologous and heterologous LPAI ex vivo by splenocytes derived from H9N2-infected chickens. The cross-reactivity of lymphocytes was tested with MHC- matched B2/B2 lung cell cultures infected with H9N2 or H7N2 LPAI. Effector:target (E:T) ratios were 10, 20 and 40 for all subjects. Standard deviation of the means was <10%. Spontaneous lysis from splenocytes derived from naive birds were <7 % against either virus (data not shown).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3108207&req=5

Figure 2: Recognition of homologous and heterologous LPAI ex vivo by splenocytes derived from H9N2-infected chickens. The cross-reactivity of lymphocytes was tested with MHC- matched B2/B2 lung cell cultures infected with H9N2 or H7N2 LPAI. Effector:target (E:T) ratios were 10, 20 and 40 for all subjects. Standard deviation of the means was <10%. Spontaneous lysis from splenocytes derived from naive birds were <7 % against either virus (data not shown).
Mentions: Splenic T cells from inbred chickens infected with H9N2 AI lysed target cells infected with either homologous or H7N2 AI at all effector:target (E:T) ratios tested (Fig 2). A dose response based on E:T ratios was observed. At E:T ratio of 40:1, 52 % of H9N2-infected B2/B2 lung target cells were lysed, while 43 % of H7N2-infected target cells were lysed. At lower E:T ratios, approximately 18 % (20:1) and 10 % (10:1) of infected target cells were lysed in either H9N2 or H7N2-infected lung cells. The splenic T cells from H9N2 infected birds did not lyse uninfected target cells, although spontaneous lysis was approximately 7 % (data not shown). In addition, lymphocytes obtained from sham-infected birds did not lyse infected or control lung cell cultures (data not shown).

Bottom Line: Cellular immunity was determined by cytotoxic lysis of B2/B2 infected lung target cells and proliferation of T cells following exposure to LPAI.Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds.T cell proliferation was determined to be highest when exposed to the homologous virus.

View Article: PubMed Central - HTML - PubMed

Affiliation: Southeast Poultry Research Laboratory, Agricultural Research Service, USA, Department of Agriculture, 934 College Station Road, Athens, GA 30605, USA. darrell.kapczynski@ars.usda.gov.

ABSTRACT

Background: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little is known about cellular immunity following a primary AI infection in poultry, especially regarding cytotoxic T lymphocytes (CTL's).

Methods: In these studies, major histocompatibility complex (MHC)-defined (B2/B2) chickens were infected with low pathogenic AI (LPAI) H9N2 and clinical signs of disease were monitored over a two weeks period. Splenic lymphocytes from infected and naïve birds were examined for cross reactivity against homologous and heterologous (H7N2) LPAI by ex vivo stimulation. Cellular immunity was determined by cytotoxic lysis of B2/B2 infected lung target cells and proliferation of T cells following exposure to LPAI.

Results: Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds. Splenic lymphocytes derived from H9N2-infected birds displayed lysis of both homologous (H9N2) and heterologous (H7N2) infected target cells, whereas lymphocytes obtained from sham-infected birds did not. T cell proliferation was determined to be highest when exposed to the homologous virus.

Conclusions: Taken together these data extend the findings that cellular immunity, including CTL's, is cross reactive against heterologous isolates of AI and contribute to protection following infection.

No MeSH data available.


Related in: MedlinePlus