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Highly pathogenic or low pathogenic avian influenza virus subtype H7N1 infection in chicken lungs: small differences in general acute responses.

Rebel JM, Peeters B, Fijten H, Post J, Cornelissen J, Vervelde L - Vet. Res. (2011)

Bottom Line: No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus.However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs.A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Veterinary Institute, PO box 65, 8219 PH Lelystad, The Netherlands. Annemarie.Rebel@WUR.nl.

ABSTRACT
Avian influenza virus can be divided into two groups, highly pathogenic avian influenza virus (HPAI) and low pathogenic avian influenza virus (LPAI) based on their difference in virulence. To investigate if the difference in clinical outcome between LPAI and HPAI in chickens is due to immunological host responses in the lung within the first 24 hours post infection (hpi), chickens were infected with LPAI or HPAI of subtype H7N1. Virus was found in the caudal and cranial part of the lung. With LPAI, virus was localised around the intrapulmonary bronchus and secondary bronchi. In sharp contrast, HPAI was detected throughout the whole lung. However, based on viral RNA levels, no quantitative difference was observed between LPAI and HPAI infected birds. In infected areas of the lungs, an influx of CD8α+ cells as well as KUL01+ macrophages and dendritic cells (DC) occurred as fast as 8 hpi in both infected groups. No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus. However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs. A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

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Detection of CD8α+ (A-C) and KUL01+ (D-E) cells in lung 16-24 h after AIV infection. In LPAI infected chickens influxes of CD8α+ cells are mainly detected in and adjacent to the intrapulmonary bronchus (A) and rarely in peripheral parabronchi (B). In HPAI infected chickens influxes of CD8α+ are also detected in peripheral parabronchi (C). Influxes of KUL01+ cells were localised in and adjacent to the intrapulmonary bronchus after infection with LPAI (D), whereas KUL01+ cells are detected in peripheral parabronchi after infection with HPAI (E). These cellular influxes co-localised with virus infected cells.
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Figure 4: Detection of CD8α+ (A-C) and KUL01+ (D-E) cells in lung 16-24 h after AIV infection. In LPAI infected chickens influxes of CD8α+ cells are mainly detected in and adjacent to the intrapulmonary bronchus (A) and rarely in peripheral parabronchi (B). In HPAI infected chickens influxes of CD8α+ are also detected in peripheral parabronchi (C). Influxes of KUL01+ cells were localised in and adjacent to the intrapulmonary bronchus after infection with LPAI (D), whereas KUL01+ cells are detected in peripheral parabronchi after infection with HPAI (E). These cellular influxes co-localised with virus infected cells.

Mentions: In uninfected birds KUL01+ cells were found scattered throughout the parabronchi and in the lamina propria of the intrapulmonary bronchus and secondary bronchi (Figure 4). Small KUL01+ cell influxes were seen in the interparabronchial septa with both LPAI and HPAI virus as early as 4 hpi, and from 8 hpi the cells changed morphologically from dendritic shape to round with the intensity of expression of KUL01 decreasing. Largest influxes were found in and around the intrapulmonary bronchus in both LPAI and HPAI virus infected birds. Increases in CD8α+ and CD4+ cells were found from 16 hpi onwards (Figure 4). Cellular influxes co-localised with virus infected areas, which resulted in the LPAI virus infected birds in more influxes in the parabronchi adjacent to the intrapulmonary bronchus, whereas in the HPAI virus infected birds influxes were also found in parabronchi closer to the airsacs.


Highly pathogenic or low pathogenic avian influenza virus subtype H7N1 infection in chicken lungs: small differences in general acute responses.

Rebel JM, Peeters B, Fijten H, Post J, Cornelissen J, Vervelde L - Vet. Res. (2011)

Detection of CD8α+ (A-C) and KUL01+ (D-E) cells in lung 16-24 h after AIV infection. In LPAI infected chickens influxes of CD8α+ cells are mainly detected in and adjacent to the intrapulmonary bronchus (A) and rarely in peripheral parabronchi (B). In HPAI infected chickens influxes of CD8α+ are also detected in peripheral parabronchi (C). Influxes of KUL01+ cells were localised in and adjacent to the intrapulmonary bronchus after infection with LPAI (D), whereas KUL01+ cells are detected in peripheral parabronchi after infection with HPAI (E). These cellular influxes co-localised with virus infected cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3037890&req=5

Figure 4: Detection of CD8α+ (A-C) and KUL01+ (D-E) cells in lung 16-24 h after AIV infection. In LPAI infected chickens influxes of CD8α+ cells are mainly detected in and adjacent to the intrapulmonary bronchus (A) and rarely in peripheral parabronchi (B). In HPAI infected chickens influxes of CD8α+ are also detected in peripheral parabronchi (C). Influxes of KUL01+ cells were localised in and adjacent to the intrapulmonary bronchus after infection with LPAI (D), whereas KUL01+ cells are detected in peripheral parabronchi after infection with HPAI (E). These cellular influxes co-localised with virus infected cells.
Mentions: In uninfected birds KUL01+ cells were found scattered throughout the parabronchi and in the lamina propria of the intrapulmonary bronchus and secondary bronchi (Figure 4). Small KUL01+ cell influxes were seen in the interparabronchial septa with both LPAI and HPAI virus as early as 4 hpi, and from 8 hpi the cells changed morphologically from dendritic shape to round with the intensity of expression of KUL01 decreasing. Largest influxes were found in and around the intrapulmonary bronchus in both LPAI and HPAI virus infected birds. Increases in CD8α+ and CD4+ cells were found from 16 hpi onwards (Figure 4). Cellular influxes co-localised with virus infected areas, which resulted in the LPAI virus infected birds in more influxes in the parabronchi adjacent to the intrapulmonary bronchus, whereas in the HPAI virus infected birds influxes were also found in parabronchi closer to the airsacs.

Bottom Line: No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus.However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs.A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

View Article: PubMed Central - HTML - PubMed

Affiliation: Central Veterinary Institute, PO box 65, 8219 PH Lelystad, The Netherlands. Annemarie.Rebel@WUR.nl.

ABSTRACT
Avian influenza virus can be divided into two groups, highly pathogenic avian influenza virus (HPAI) and low pathogenic avian influenza virus (LPAI) based on their difference in virulence. To investigate if the difference in clinical outcome between LPAI and HPAI in chickens is due to immunological host responses in the lung within the first 24 hours post infection (hpi), chickens were infected with LPAI or HPAI of subtype H7N1. Virus was found in the caudal and cranial part of the lung. With LPAI, virus was localised around the intrapulmonary bronchus and secondary bronchi. In sharp contrast, HPAI was detected throughout the whole lung. However, based on viral RNA levels, no quantitative difference was observed between LPAI and HPAI infected birds. In infected areas of the lungs, an influx of CD8α+ cells as well as KUL01+ macrophages and dendritic cells (DC) occurred as fast as 8 hpi in both infected groups. No major difference between LPAI and HPAI infected birds in the induction of cytokines and interferons at mRNA level in lung tissue was found.In conclusion, the differences in lethality for chickens infected with LPAI or HPAI could be ascribed to difference in location of the virus. However similar amounts of viral RNA, similar cytokine mRNA levels, and similar influxes of CD8α+ and KUL01+ macrophages and DC were found between HPAI and LPAI in the lungs. A cytokine storm at mRNA level as described for mammals was not observed in the lungs of HPAI infected birds within 24 hpi.

Show MeSH
Related in: MedlinePlus