Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury
Background : Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF- α ) and interleu...
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| creator | Hermsen, Joshua L. Sano, Yoshifumi Gomez, F. Enrique Maeshima, Yoshinori Kang, Woodae Kudsk, Kenneth A. |
| description | Background
: Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF-
α
) and interleukin-1 beta (IL-1
β
) stimulate the production of polymeric immunoglobulin receptor (pIgR), the protein required to transport immunoglobulin A (IgA) to mucosal surfaces. We have shown that PN alters levels of lung and nasal passage IgA and several IgA-stimulating cytokines. We hypothesized that TNF-
α
and IL-1
β
blockade, as well as PN, would blunt the airway IgA response to injury.
Methods
: Male Institute of Cancer Research (ICR) mice were randomized to uninjured controls (n = 10) or to intra-peritoneal phosphate-buffered saline (PBS) (n = 9), antagonistic TNF-
α
antibody (100 mcg, n = 7), or antagonistic IL-1
β
antibody (50 mcg, n = 8) 30 min prior to surgical stress with laparotomy and neck incisions. Mice were sacrificed at 8 h for nasal and bronchoalveolar lavage (NAL, BAL) to measure IgA by enzyme-linked immunosorbent assay. In a separate experiment, 12 mice underwent intravenous cannulation followed by chow (n = 5) or PN (n = 7) feeding for 5 days prior to the same stress and IgA measurement.
Results
: Injury significantly increased NAL and BAL IgA (225 ± 104 ng) compared with baseline (145 ± 38 ng; p = 0.01). Blockade of TNF-
α
eliminated the innate airway IgA response to injury (130 ± 47 ng; p = 0.01), whereas IL-1
β
blockade blunted and PN eliminated it completely.
Conclusions
: Tumor necrosis factor-alpha is involved in the respiratory IgA immune response to injury. Both TNF-
α
blockade and PN impair this innate response, and blockade of IL-1
β
impairs it to a degree. We hypothesize that these cytokines blunt this response via their known effects on the polymeric immunoglobulin receptor (pIgR), whereas the PN-induced deficit likely is multifactorial. |
| doi_str_mv | 10.1089/sur.2007.029 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_70427630</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A179695570</galeid><sourcerecordid>A179695570</sourcerecordid><originalsourceid>FETCH-LOGICAL-c391t-3a651b5b19457945e96240387805414d141b976a9ac28bc3fc0cf491a8f36ce93</originalsourceid><addsrcrecordid>eNptkc9q3DAQh0Vpaf60t56DodBDiTeSJUvWcVmaZCFNQ0lyFbI8ThRsaSPJhzxWXqTPFJldUgJBCInh-w3DfAh9I3hBcCNP4hQWFcZigSv5Ae2TuhZlwwX7mP9Y8rKSnO2hgxgfMCai4vwz2iMN5ZRxvo9ur3QAlyDoobicUrDJeles3b1tbYrF9TT6UFyCCT7aWJxqk3wo_z2Xv6GzOkFXrO-WxV-IG-8iFMnn6MMUnr6gT70eInzdvYfo5vTX9eq8vPhztl4tL0pDJUkl1bwmbd0SyWqRL0heMUwb0eCaEdYRRlopuJbaVE1raG-w6ZkkuukpNyDpIfqx7bsJ_nGCmNRoo4Fh0A78FJXArBKc4gx-34J3egBlXe9T0GaG1ZIIyWVe20wt3qHy6WC0xjvoba6_CRxvA_OCYoBebYIddXhSBKtZj8p61KxHZT0ZP9qNO7UjdP_hnY8M_NwCc1k7N1hoIaRX8E23F4O5mNc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>70427630</pqid></control><display><type>article</type><title>Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Hermsen, Joshua L. ; Sano, Yoshifumi ; Gomez, F. Enrique ; Maeshima, Yoshinori ; Kang, Woodae ; Kudsk, Kenneth A.</creator><creatorcontrib>Hermsen, Joshua L. ; Sano, Yoshifumi ; Gomez, F. Enrique ; Maeshima, Yoshinori ; Kang, Woodae ; Kudsk, Kenneth A.</creatorcontrib><description>Background
: Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF-
α
) and interleukin-1 beta (IL-1
β
) stimulate the production of polymeric immunoglobulin receptor (pIgR), the protein required to transport immunoglobulin A (IgA) to mucosal surfaces. We have shown that PN alters levels of lung and nasal passage IgA and several IgA-stimulating cytokines. We hypothesized that TNF-
α
and IL-1
β
blockade, as well as PN, would blunt the airway IgA response to injury.
Methods
: Male Institute of Cancer Research (ICR) mice were randomized to uninjured controls (n = 10) or to intra-peritoneal phosphate-buffered saline (PBS) (n = 9), antagonistic TNF-
α
antibody (100 mcg, n = 7), or antagonistic IL-1
β
antibody (50 mcg, n = 8) 30 min prior to surgical stress with laparotomy and neck incisions. Mice were sacrificed at 8 h for nasal and bronchoalveolar lavage (NAL, BAL) to measure IgA by enzyme-linked immunosorbent assay. In a separate experiment, 12 mice underwent intravenous cannulation followed by chow (n = 5) or PN (n = 7) feeding for 5 days prior to the same stress and IgA measurement.
Results
: Injury significantly increased NAL and BAL IgA (225 ± 104 ng) compared with baseline (145 ± 38 ng; p = 0.01). Blockade of TNF-
α
eliminated the innate airway IgA response to injury (130 ± 47 ng; p = 0.01), whereas IL-1
β
blockade blunted and PN eliminated it completely.
Conclusions
: Tumor necrosis factor-alpha is involved in the respiratory IgA immune response to injury. Both TNF-
α
blockade and PN impair this innate response, and blockade of IL-1
β
impairs it to a degree. We hypothesize that these cytokines blunt this response via their known effects on the polymeric immunoglobulin receptor (pIgR), whereas the PN-induced deficit likely is multifactorial.</description><identifier>ISSN: 1096-2964</identifier><identifier>EISSN: 1557-8674</identifier><identifier>DOI: 10.1089/sur.2007.029</identifier><identifier>PMID: 18363466</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Animals ; Bronchoalveolar Lavage Fluid - immunology ; Diagnosis ; Enzyme-Linked Immunosorbent Assay ; Health aspects ; Immunoglobulin A - immunology ; Interleukin-1beta - antagonists & inhibitors ; Interleukin-1beta - immunology ; Lung - immunology ; Lung diseases ; Male ; Mice ; Mice, Inbred ICR ; Nasal Lavage Fluid - immunology ; PAPERS FROM THE SURGICAL INFECTION SOCIETY MEETINGS ; Parenteral feeding ; Parenteral Nutrition ; Parenteral therapy ; Risk factors ; Tumor necrosis factor ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - immunology ; Wounds and Injuries - immunology</subject><ispartof>Surgical infections, 2008-02, Vol.9 (1), p.33-40</ispartof><rights>2008 Mary Ann Liebert, Inc.</rights><rights>COPYRIGHT 2008 Mary Ann Liebert, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-3a651b5b19457945e96240387805414d141b976a9ac28bc3fc0cf491a8f36ce93</citedby><cites>FETCH-LOGICAL-c391t-3a651b5b19457945e96240387805414d141b976a9ac28bc3fc0cf491a8f36ce93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18363466$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hermsen, Joshua L.</creatorcontrib><creatorcontrib>Sano, Yoshifumi</creatorcontrib><creatorcontrib>Gomez, F. Enrique</creatorcontrib><creatorcontrib>Maeshima, Yoshinori</creatorcontrib><creatorcontrib>Kang, Woodae</creatorcontrib><creatorcontrib>Kudsk, Kenneth A.</creatorcontrib><title>Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury</title><title>Surgical infections</title><addtitle>Surg Infect (Larchmt)</addtitle><description>Background
: Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF-
α
) and interleukin-1 beta (IL-1
β
) stimulate the production of polymeric immunoglobulin receptor (pIgR), the protein required to transport immunoglobulin A (IgA) to mucosal surfaces. We have shown that PN alters levels of lung and nasal passage IgA and several IgA-stimulating cytokines. We hypothesized that TNF-
α
and IL-1
β
blockade, as well as PN, would blunt the airway IgA response to injury.
Methods
: Male Institute of Cancer Research (ICR) mice were randomized to uninjured controls (n = 10) or to intra-peritoneal phosphate-buffered saline (PBS) (n = 9), antagonistic TNF-
α
antibody (100 mcg, n = 7), or antagonistic IL-1
β
antibody (50 mcg, n = 8) 30 min prior to surgical stress with laparotomy and neck incisions. Mice were sacrificed at 8 h for nasal and bronchoalveolar lavage (NAL, BAL) to measure IgA by enzyme-linked immunosorbent assay. In a separate experiment, 12 mice underwent intravenous cannulation followed by chow (n = 5) or PN (n = 7) feeding for 5 days prior to the same stress and IgA measurement.
Results
: Injury significantly increased NAL and BAL IgA (225 ± 104 ng) compared with baseline (145 ± 38 ng; p = 0.01). Blockade of TNF-
α
eliminated the innate airway IgA response to injury (130 ± 47 ng; p = 0.01), whereas IL-1
β
blockade blunted and PN eliminated it completely.
Conclusions
: Tumor necrosis factor-alpha is involved in the respiratory IgA immune response to injury. Both TNF-
α
blockade and PN impair this innate response, and blockade of IL-1
β
impairs it to a degree. We hypothesize that these cytokines blunt this response via their known effects on the polymeric immunoglobulin receptor (pIgR), whereas the PN-induced deficit likely is multifactorial.</description><subject>Animals</subject><subject>Bronchoalveolar Lavage Fluid - immunology</subject><subject>Diagnosis</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Health aspects</subject><subject>Immunoglobulin A - immunology</subject><subject>Interleukin-1beta - antagonists & inhibitors</subject><subject>Interleukin-1beta - immunology</subject><subject>Lung - immunology</subject><subject>Lung diseases</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Nasal Lavage Fluid - immunology</subject><subject>PAPERS FROM THE SURGICAL INFECTION SOCIETY MEETINGS</subject><subject>Parenteral feeding</subject><subject>Parenteral Nutrition</subject><subject>Parenteral therapy</subject><subject>Risk factors</subject><subject>Tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><subject>Wounds and Injuries - immunology</subject><issn>1096-2964</issn><issn>1557-8674</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkc9q3DAQh0Vpaf60t56DodBDiTeSJUvWcVmaZCFNQ0lyFbI8ThRsaSPJhzxWXqTPFJldUgJBCInh-w3DfAh9I3hBcCNP4hQWFcZigSv5Ae2TuhZlwwX7mP9Y8rKSnO2hgxgfMCai4vwz2iMN5ZRxvo9ur3QAlyDoobicUrDJeles3b1tbYrF9TT6UFyCCT7aWJxqk3wo_z2Xv6GzOkFXrO-WxV-IG-8iFMnn6MMUnr6gT70eInzdvYfo5vTX9eq8vPhztl4tL0pDJUkl1bwmbd0SyWqRL0heMUwb0eCaEdYRRlopuJbaVE1raG-w6ZkkuukpNyDpIfqx7bsJ_nGCmNRoo4Fh0A78FJXArBKc4gx-34J3egBlXe9T0GaG1ZIIyWVe20wt3qHy6WC0xjvoba6_CRxvA_OCYoBebYIddXhSBKtZj8p61KxHZT0ZP9qNO7UjdP_hnY8M_NwCc1k7N1hoIaRX8E23F4O5mNc</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Hermsen, Joshua L.</creator><creator>Sano, Yoshifumi</creator><creator>Gomez, F. Enrique</creator><creator>Maeshima, Yoshinori</creator><creator>Kang, Woodae</creator><creator>Kudsk, Kenneth A.</creator><general>Mary Ann Liebert, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20080201</creationdate><title>Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury</title><author>Hermsen, Joshua L. ; Sano, Yoshifumi ; Gomez, F. Enrique ; Maeshima, Yoshinori ; Kang, Woodae ; Kudsk, Kenneth A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-3a651b5b19457945e96240387805414d141b976a9ac28bc3fc0cf491a8f36ce93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Bronchoalveolar Lavage Fluid - immunology</topic><topic>Diagnosis</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Health aspects</topic><topic>Immunoglobulin A - immunology</topic><topic>Interleukin-1beta - antagonists & inhibitors</topic><topic>Interleukin-1beta - immunology</topic><topic>Lung - immunology</topic><topic>Lung diseases</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Nasal Lavage Fluid - immunology</topic><topic>PAPERS FROM THE SURGICAL INFECTION SOCIETY MEETINGS</topic><topic>Parenteral feeding</topic><topic>Parenteral Nutrition</topic><topic>Parenteral therapy</topic><topic>Risk factors</topic><topic>Tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><topic>Wounds and Injuries - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hermsen, Joshua L.</creatorcontrib><creatorcontrib>Sano, Yoshifumi</creatorcontrib><creatorcontrib>Gomez, F. Enrique</creatorcontrib><creatorcontrib>Maeshima, Yoshinori</creatorcontrib><creatorcontrib>Kang, Woodae</creatorcontrib><creatorcontrib>Kudsk, Kenneth A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Surgical infections</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hermsen, Joshua L.</au><au>Sano, Yoshifumi</au><au>Gomez, F. Enrique</au><au>Maeshima, Yoshinori</au><au>Kang, Woodae</au><au>Kudsk, Kenneth A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury</atitle><jtitle>Surgical infections</jtitle><addtitle>Surg Infect (Larchmt)</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>9</volume><issue>1</issue><spage>33</spage><epage>40</epage><pages>33-40</pages><issn>1096-2964</issn><eissn>1557-8674</eissn><abstract>Background
: Parenteral nutrition (PN) increases the incidence of pneumonia in severely injured patients compared with enteral feeding (ENT). Injury induces an innate airway IgA response in severely injured patients; similar responses occur in mice. Tumor necrosis factor-alpha (TNF-
α
) and interleukin-1 beta (IL-1
β
) stimulate the production of polymeric immunoglobulin receptor (pIgR), the protein required to transport immunoglobulin A (IgA) to mucosal surfaces. We have shown that PN alters levels of lung and nasal passage IgA and several IgA-stimulating cytokines. We hypothesized that TNF-
α
and IL-1
β
blockade, as well as PN, would blunt the airway IgA response to injury.
Methods
: Male Institute of Cancer Research (ICR) mice were randomized to uninjured controls (n = 10) or to intra-peritoneal phosphate-buffered saline (PBS) (n = 9), antagonistic TNF-
α
antibody (100 mcg, n = 7), or antagonistic IL-1
β
antibody (50 mcg, n = 8) 30 min prior to surgical stress with laparotomy and neck incisions. Mice were sacrificed at 8 h for nasal and bronchoalveolar lavage (NAL, BAL) to measure IgA by enzyme-linked immunosorbent assay. In a separate experiment, 12 mice underwent intravenous cannulation followed by chow (n = 5) or PN (n = 7) feeding for 5 days prior to the same stress and IgA measurement.
Results
: Injury significantly increased NAL and BAL IgA (225 ± 104 ng) compared with baseline (145 ± 38 ng; p = 0.01). Blockade of TNF-
α
eliminated the innate airway IgA response to injury (130 ± 47 ng; p = 0.01), whereas IL-1
β
blockade blunted and PN eliminated it completely.
Conclusions
: Tumor necrosis factor-alpha is involved in the respiratory IgA immune response to injury. Both TNF-
α
blockade and PN impair this innate response, and blockade of IL-1
β
impairs it to a degree. We hypothesize that these cytokines blunt this response via their known effects on the polymeric immunoglobulin receptor (pIgR), whereas the PN-induced deficit likely is multifactorial.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>18363466</pmid><doi>10.1089/sur.2007.029</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1096-2964 |
| ispartof | Surgical infections, 2008-02, Vol.9 (1), p.33-40 |
| issn | 1096-2964 1557-8674 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70427630 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals Bronchoalveolar Lavage Fluid - immunology Diagnosis Enzyme-Linked Immunosorbent Assay Health aspects Immunoglobulin A - immunology Interleukin-1beta - antagonists & inhibitors Interleukin-1beta - immunology Lung - immunology Lung diseases Male Mice Mice, Inbred ICR Nasal Lavage Fluid - immunology PAPERS FROM THE SURGICAL INFECTION SOCIETY MEETINGS Parenteral feeding Parenteral Nutrition Parenteral therapy Risk factors Tumor necrosis factor Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - immunology Wounds and Injuries - immunology |
| title | Parenteral Nutrition Inhibits Tumor Necrosis Factor-α-Mediated IgA Response to Injury |
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