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Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats
The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\Fe-deficient weanling SD rats. Rats...
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Published in: | Journal of immunotoxicology 2020-01, Vol.17 (1), p.144-152 |
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description | The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\Fe-deficient weanling SD rats. Rats were fed a control (CD) or Fe-deficient (ID) diet for 4 weeks and then evaluated for hemoglobin (Hb) and serum Fe status. Then, half the rats in each group began to receive daily oral Pb exposure (25 mg/4 ml/kg BW; gavage) or vehicle for a further 4 weeks (while maintained on original respective diets). After the 4-weeks of dosing, rats were assessed for Hb and serum Fe, and for blood lead level (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity. At this point, half the rats in each group (now n = 8) were then vaccinated with tetanus toxoid (TT), and then two boosters at 2-week intervals. All the time, rats stayed on their original respective diets along with exposure to Pb on alternate days. At 2 weeks after the final booster, rats were euthanized and blood collected to assess total/specific IgG and IgM levels; mucosal (intestinal) IgA levels were also determined. Spleens were taken to assess CD4
+
and CD8
+
cell levels and for ex vivo measures of splenocyte proliferation/T
H
1 and T
H
2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4
+
cell levels were not impacted by treatment; CD8
+
levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes. |
doi_str_mv | 10.1080/1547691X.2020.1773973 |
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+
and CD8
+
cell levels and for ex vivo measures of splenocyte proliferation/T
H
1 and T
H
2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4
+
cell levels were not impacted by treatment; CD8
+
levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes.</description><identifier>ISSN: 1547-691X</identifier><identifier>EISSN: 1547-6901</identifier><identifier>DOI: 10.1080/1547691X.2020.1773973</identifier><language>eng</language><publisher>Abingdon: Taylor & Francis</publisher><subject>Aminolevulinic acid ; Blood ; CD4 antigen ; CD8 antigen ; Cytokines ; Developing countries ; Diet ; Hemoglobin ; Immune response (humoral) ; Immune system ; Immunoglobulin A ; Immunoglobulin G ; Immunoglobulin M ; Intestine ; Iron ; Iron deficiency ; LDCs ; Lead ; Lymphocytes T ; Mucosal immunity ; Nutrient deficiency ; Rodents ; splenocyte proliferation index ; Tetanus ; th1 ; th2 ; Toxicity ; vaccination ; Vaccines</subject><ispartof>Journal of immunotoxicology, 2020-01, Vol.17 (1), p.144-152</ispartof><rights>2020 ICMR - NATIONAL INSTITUTE OF NUTRITION, GOI, HYDERABAD INDIA. Published by Informa UK Limited, trading as Taylor & Francis Group. 2020</rights><rights>2020 ICMR - NATIONAL INSTITUTE OF NUTRITION, GOI, HYDERABAD INDIA. Published by Informa UK Limited, trading as Taylor & Francis Group. This work is licensed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-2eff0734b0a2be29f95541e4c49e31d73d5fe3dcf48453d53465b111fcd97d973</citedby><cites>FETCH-LOGICAL-c484t-2eff0734b0a2be29f95541e4c49e31d73d5fe3dcf48453d53465b111fcd97d973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/1547691X.2020.1773973$$EPDF$$P50$$Ginformaworld$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2474255495?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27502,27924,27925,37012,44590,59143,59144</link.rule.ids></links><search><creatorcontrib>Yathapu, Srinivasa Reddy</creatorcontrib><creatorcontrib>Kondapalli, Narendra Babu</creatorcontrib><creatorcontrib>Srivalliputturu, Sarath Babu</creatorcontrib><creatorcontrib>Hemalatha, Rajkumar</creatorcontrib><creatorcontrib>Bharatraj, Dinesh Kumar</creatorcontrib><title>Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats</title><title>Journal of immunotoxicology</title><description>The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\Fe-deficient weanling SD rats. Rats were fed a control (CD) or Fe-deficient (ID) diet for 4 weeks and then evaluated for hemoglobin (Hb) and serum Fe status. Then, half the rats in each group began to receive daily oral Pb exposure (25 mg/4 ml/kg BW; gavage) or vehicle for a further 4 weeks (while maintained on original respective diets). After the 4-weeks of dosing, rats were assessed for Hb and serum Fe, and for blood lead level (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity. At this point, half the rats in each group (now n = 8) were then vaccinated with tetanus toxoid (TT), and then two boosters at 2-week intervals. All the time, rats stayed on their original respective diets along with exposure to Pb on alternate days. At 2 weeks after the final booster, rats were euthanized and blood collected to assess total/specific IgG and IgM levels; mucosal (intestinal) IgA levels were also determined. Spleens were taken to assess CD4
+
and CD8
+
cell levels and for ex vivo measures of splenocyte proliferation/T
H
1 and T
H
2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4
+
cell levels were not impacted by treatment; CD8
+
levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes.</description><subject>Aminolevulinic acid</subject><subject>Blood</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Cytokines</subject><subject>Developing countries</subject><subject>Diet</subject><subject>Hemoglobin</subject><subject>Immune response (humoral)</subject><subject>Immune system</subject><subject>Immunoglobulin A</subject><subject>Immunoglobulin G</subject><subject>Immunoglobulin M</subject><subject>Intestine</subject><subject>Iron</subject><subject>Iron deficiency</subject><subject>LDCs</subject><subject>Lead</subject><subject>Lymphocytes T</subject><subject>Mucosal immunity</subject><subject>Nutrient deficiency</subject><subject>Rodents</subject><subject>splenocyte proliferation index</subject><subject>Tetanus</subject><subject>th1</subject><subject>th2</subject><subject>Toxicity</subject><subject>vaccination</subject><subject>Vaccines</subject><issn>1547-691X</issn><issn>1547-6901</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kV9rFTEQxRdRsFY_ghDweWv-7e6NT5bSaqHgi0LfQm4yU3PZTa6TrHq_vbne2kchMMnhzG_CnK57K_iF4Bv-Xgx6Go24v5BcNmmalJnUs-7sqPej4eL5013cv-xelbLjXBqh-Fm3XCOCrywjm8EFBr_3uawEzKXA0lop1piTm1mknPoAGH2E5A8sJxaXZU3ACMo-pwIf2CX76byPTfPf3TxDegBW6hoOLCZGrpbX3Qt0c4E3j_W8-3Zz_fXqc3_35dPt1eVd7_VG114CIp-U3nIntyANmmHQArTXBpQIkwoDggoem3toD6XHYSuEQB_M1I46725P3JDdzu4pLo4ONrto_wqZHqyjGv0M1m04YhhNYzSYGY3zYeQbLVHxsBW-sd6dWHvKP1Yo1e7ySm0lxUo9adm-ZobmGk4uT7kUAnyaKrg9pmT_pWSPKdnHlFrfx1NfTJhpcb8yzcFWd5gzIbnkY7Hq_4g_qbCZ1Q</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Yathapu, Srinivasa Reddy</creator><creator>Kondapalli, Narendra Babu</creator><creator>Srivalliputturu, Sarath Babu</creator><creator>Hemalatha, Rajkumar</creator><creator>Bharatraj, Dinesh Kumar</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><general>Taylor & Francis Group</general><scope>0YH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>DOA</scope></search><sort><creationdate>20200101</creationdate><title>Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats</title><author>Yathapu, Srinivasa Reddy ; Kondapalli, Narendra Babu ; Srivalliputturu, Sarath Babu ; Hemalatha, Rajkumar ; Bharatraj, Dinesh Kumar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c484t-2eff0734b0a2be29f95541e4c49e31d73d5fe3dcf48453d53465b111fcd97d973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aminolevulinic acid</topic><topic>Blood</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>Cytokines</topic><topic>Developing countries</topic><topic>Diet</topic><topic>Hemoglobin</topic><topic>Immune response (humoral)</topic><topic>Immune system</topic><topic>Immunoglobulin A</topic><topic>Immunoglobulin G</topic><topic>Immunoglobulin M</topic><topic>Intestine</topic><topic>Iron</topic><topic>Iron deficiency</topic><topic>LDCs</topic><topic>Lead</topic><topic>Lymphocytes T</topic><topic>Mucosal immunity</topic><topic>Nutrient deficiency</topic><topic>Rodents</topic><topic>splenocyte proliferation index</topic><topic>Tetanus</topic><topic>th1</topic><topic>th2</topic><topic>Toxicity</topic><topic>vaccination</topic><topic>Vaccines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yathapu, Srinivasa Reddy</creatorcontrib><creatorcontrib>Kondapalli, Narendra Babu</creatorcontrib><creatorcontrib>Srivalliputturu, Sarath Babu</creatorcontrib><creatorcontrib>Hemalatha, Rajkumar</creatorcontrib><creatorcontrib>Bharatraj, Dinesh Kumar</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Directory of Open Access Journals</collection><jtitle>Journal of immunotoxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yathapu, Srinivasa Reddy</au><au>Kondapalli, Narendra Babu</au><au>Srivalliputturu, Sarath Babu</au><au>Hemalatha, Rajkumar</au><au>Bharatraj, Dinesh Kumar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats</atitle><jtitle>Journal of immunotoxicology</jtitle><date>2020-01-01</date><risdate>2020</risdate><volume>17</volume><issue>1</issue><spage>144</spage><epage>152</epage><pages>144-152</pages><issn>1547-691X</issn><eissn>1547-6901</eissn><abstract>The prevalence of iron (Fe) deficiency and subclinical lead (Pb) toxicity is high in developing countries like India, and information on their potential additive effects on immune responses is scant. The current study assessed immune parameters in dual Pb-exposed\Fe-deficient weanling SD rats. Rats were fed a control (CD) or Fe-deficient (ID) diet for 4 weeks and then evaluated for hemoglobin (Hb) and serum Fe status. Then, half the rats in each group began to receive daily oral Pb exposure (25 mg/4 ml/kg BW; gavage) or vehicle for a further 4 weeks (while maintained on original respective diets). After the 4-weeks of dosing, rats were assessed for Hb and serum Fe, and for blood lead level (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity. At this point, half the rats in each group (now n = 8) were then vaccinated with tetanus toxoid (TT), and then two boosters at 2-week intervals. All the time, rats stayed on their original respective diets along with exposure to Pb on alternate days. At 2 weeks after the final booster, rats were euthanized and blood collected to assess total/specific IgG and IgM levels; mucosal (intestinal) IgA levels were also determined. Spleens were taken to assess CD4
+
and CD8
+
cell levels and for ex vivo measures of splenocyte proliferation/T
H
1 and T
H
2 cytokine formation. The results indicated significant lowering of Hb and serum Fe levels in ID rats and increased blood Pb and decreased ALAD activity in all Pb-exposed rats. Fe-deficiency alone induced significant increases in ALAD activity, but only in an absence of Pb. While there was no impact of any regimen on total or TT-specific IgG, significant decreases in mucosal IgA and TT-specific IgM were seen in ID-fed Pb-exposed rats. CD4
+
cell levels were not impacted by treatment; CD8
+
levels were increased in all ID/Pb-exposed rats. Ex-vivo splenocyte proliferation was significantly higher among vaccinated rats, as well as ID-fed Pb-exposed unvaccinated rats. Cytokine formation in all cases was highly variable. The results suggest that Fe deficiency compromised cell-mediated, mucosal, and/or humoral immune response-related endpoints and that Pb exposure during the deficiency further impacted these outcomes.</abstract><cop>Abingdon</cop><pub>Taylor & Francis</pub><doi>10.1080/1547691X.2020.1773973</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aminolevulinic acid Blood CD4 antigen CD8 antigen Cytokines Developing countries Diet Hemoglobin Immune response (humoral) Immune system Immunoglobulin A Immunoglobulin G Immunoglobulin M Intestine Iron Iron deficiency LDCs Lead Lymphocytes T Mucosal immunity Nutrient deficiency Rodents splenocyte proliferation index Tetanus th1 th2 Toxicity vaccination Vaccines |
title | Effect of lead exposure and nutritional iron-deficiency on immune response: A vaccine challenge study in rats |
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