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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

Lymphocyte proliferation responses induced by H9N2 infection in MHC-defined chickens against homologous and heterologous AI. Groups of chickens received either sham or H9N2 infection. Spleens of individual birds were removed, and lymphocyte proliferation was evaluated using the alamarBlue™ method. Samples were read at 48 hours and the percent alamarBlue™ reduced, as an indicator of proliferation, presented per group. Proliferation by lymphocytes from sham birds against either AI virus was <12 % (data not shown).
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Figure 3: Lymphocyte proliferation responses induced by H9N2 infection in MHC-defined chickens against homologous and heterologous AI. Groups of chickens received either sham or H9N2 infection. Spleens of individual birds were removed, and lymphocyte proliferation was evaluated using the alamarBlue™ method. Samples were read at 48 hours and the percent alamarBlue™ reduced, as an indicator of proliferation, presented per group. Proliferation by lymphocytes from sham birds against either AI virus was <12 % (data not shown).

Mentions: Splenocytes from H9N2 infected birds were tested for CMI memory response against homologous and heterologous AI via lymphocyte proliferative. The results (Fig. 3) indicate an increased proliferation response, as determined as an increase in the percent of alamaBlue™ reduced by the lymphocytes, against both the H9N2 and H7N2 virus. The highest proliferative response was against the homologous virus (42%), which was less than the response to the T-cell mitogen, concanavalin A (ConA). The T cell proliferative response to the heterologous virus was approximately half (25%) of that observed against the homologous virus.


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)

Lymphocyte proliferation responses induced by H9N2 infection in MHC-defined chickens against homologous and heterologous AI. Groups of chickens received either sham or H9N2 infection. Spleens of individual birds were removed, and lymphocyte proliferation was evaluated using the alamarBlue™ method. Samples were read at 48 hours and the percent alamarBlue™ reduced, as an indicator of proliferation, presented per group. Proliferation by lymphocytes from sham birds against either AI virus was <12 % (data not shown).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: Lymphocyte proliferation responses induced by H9N2 infection in MHC-defined chickens against homologous and heterologous AI. Groups of chickens received either sham or H9N2 infection. Spleens of individual birds were removed, and lymphocyte proliferation was evaluated using the alamarBlue™ method. Samples were read at 48 hours and the percent alamarBlue™ reduced, as an indicator of proliferation, presented per group. Proliferation by lymphocytes from sham birds against either AI virus was <12 % (data not shown).
Mentions: Splenocytes from H9N2 infected birds were tested for CMI memory response against homologous and heterologous AI via lymphocyte proliferative. The results (Fig. 3) indicate an increased proliferation response, as determined as an increase in the percent of alamaBlue™ reduced by the lymphocytes, against both the H9N2 and H7N2 virus. The highest proliferative response was against the homologous virus (42%), which was less than the response to the T-cell mitogen, concanavalin A (ConA). The T cell proliferative response to the heterologous virus was approximately half (25%) of that observed against the homologous virus.

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