ABSTRACT Background:Chronicobstructivepulmonarydisease(COPD)isachronicprogressiveinflammatorydiseasecharacterizedbylimitationsairflowthatisnotfullyreversible(42).ThepathophysiologyofCOPDisnotcompletelyunderstood. Cigarettesmoking is amajorriskfactorforchronicobstructivepulmonarydisease(COPD).ElevatedCRPhasbeenincreasinglyusedasasurrogatemarkerofsystemicinflammationindiverseconditions.TNF-α,apowerfulpro-inflammatorycytokineprimarilyproducedbyactivatedmacrophages,isthoughttoacriticalroleinthepathogenesisofCOPD[13,14]. Theaimofthework:toevaluatetheimpactofsmokingoninflamatorybiomarkersandrelationsbetweenthesebiomarkersandthedeclineoflungfunctioninCOPDpatients. Methods:Thiscase–controlobservationalprospectivestudywasconductedonfifty-eightclinicallystableCOPDpatients(26non-smokersand32current smokers;at differentstagesrangedfrommildtoverysevere),theirmeanage53.1±14.25and53.9±5.95yearsrespectively),recruitedfromChestDepartment,AssiutUniversityHospitals.AllpatientsmettheGlobalInitiativeforObstructiveLungDisease(GOLD)[4].Allparticipantsweresubjectedtothoroughhistorytaking,fullclinicalexamination,anthropometricmeasurementswithspirometryandchest X-ray.Peripheralhemogram,liverfunctiontests,kidneyfunctiontests,highsensitivityC-reactiveprotein(hsCRP)andserumlevelofTNF-αweremeasuredforbothpatientsandcontrols. Results:Theconcentrationsofcirculatinghs-CRPandTNF-α,werehighlysignificantlyelevatedinpatientswithCOPDincomparisontothecontrolgroup(3.74±0.2vs.1.30±0.14forhs-CRP;33.88±5.97vs.8.79±0.57forTNF-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)withnosignificantdifferenceforthemeasuredhs-CRP(3.87±0.29versus 3.58±0.27withp˃0.05).Interestingly,therewere significant negativecorrelationsbetweenthelevelsofTNF-αand hs-CRP,andFEV1instagesII,III,IVofCOPD. Conclusions:Thecirculatinglevelsoftheinflammatorymarkershs-CRPandTNF-alphaaresignificantlyelevatedinpatientswithstableCOPDandthesebiomarkerscouldbeusedaspredictorfactorsforseverityofinflammationinCOPDpatients..Longitudinalstudiesevaluatingtheeffectsofsmokingcessationonbronchialandsystemicinflammationareneededtoallowbetterunderstandingoftheserelationshipsandtheirconsequences. Keywords:COPD,FEV1,inflammatorymarkers;hs-CRPandTNF-alpha.

ABSTRACT Background:Chronicobstructivepulmonarydisease(COPD)isachronicprogressiveinflammatorydiseasecharacterizedbylimitationsairflowthatisnotfullyreversible(42).ThepathophysiologyofCOPDisnotcompletelyunderstood. Cigarettesmoking is amajorriskfactorforchronicobstructivepulmonarydisease(COPD).ElevatedCRPhasbeenincreasinglyusedasasurrogatemarkerofsystemicinflammationindiverseconditions.TNF-α,apowerfulpro-inflammatorycytokineprimarilyproducedbyactivatedmacrophages,isthoughttoacriticalroleinthepathogenesisofCOPD[13,14]. Theaimofthework:toevaluatetheimpactofsmokingoninflamatorybiomarkersandrelationsbetweenthesebiomarkersandthedeclineoflungfunctioninCOPDpatients. Methods:Thiscase–controlobservationalprospectivestudywasconductedonfifty-eightclinicallystableCOPDpatients(26non-smokersand32current smokers;at differentstagesrangedfrommildtoverysevere),theirmeanage53.1±14.25and53.9±5.95yearsrespectively),recruitedfromChestDepartment,AssiutUniversityHospitals.AllpatientsmettheGlobalInitiativeforObstructiveLungDisease(GOLD)[4].Allparticipantsweresubjectedtothoroughhistorytaking,fullclinicalexamination,anthropometricmeasurementswithspirometryandchest X-ray.Peripheralhemogram,liverfunctiontests,kidneyfunctiontests,highsensitivityC-reactiveprotein(hsCRP)andserumlevelofTNF-αweremeasuredforbothpatientsandcontrols. Results:Theconcentrationsofcirculatinghs-CRPandTNF-α,werehighlysignificantlyelevatedinpatientswithCOPDincomparisontothecontrolgroup(3.74±0.2vs.1.30±0.14forhs-CRP;33.88±5.97vs.8.79±0.57forTNF-αwithp0.0001foreach)andthelevelsofmeasuredTNF-αweresignificantlyincreasedwiththeincreaseddegreeandseverityofCOPDandincreasedseverityofsmokingstatus.RegardingthesmokingstatusofCOPDpatients,therewasahighlysignificantlydifferencefor the measuredTNF-α(53.74±9.52versus12.73±1.20withp0.0001)withnosignificantdifferenceforthemeasuredhs-CRP(3.87±0.29versus 3.58±0.27withp˃0.05).Interestingly,therewere significant negativecorrelationsbetweenthelevelsofTNF-αand hs-CRP,andFEV1instagesII,III,IVofCOPD. Conclusions:Thecirculatinglevelsoftheinflammatorymarkershs-CRPandTNF-alphaaresignificantlyelevatedinpatientswithstableCOPDandthesebiomarkerscouldbeusedaspredictorfactorsforseverityofinflammationinCOPDpatients..Longitudinalstudiesevaluatingtheeffectsofsmokingcessationonbronchialandsystemicinflammationareneededtoallowbetterunderstandingoftheserelationshipsandtheirconsequences. Keywords:COPD,FEV1,inflammatorymarkers;hs-CRPandTNF-alpha.

AbstractContinuouspositiveairwaypressure(CPAP)isastandardtreatmentofmoderateandsevereobstructive sleepapnea syndrome.However, itseffect inpatients with coexistingobstructiveandcentralapneasiscontroversial. Objectives:TodeterminetheimmediateresponsetoCPAPincombinedobstructiveandcentralsleepapneapatientswithoutheartfailure. Methods:Thirty sevenconsecutivepatients with moderateandsevere coexisting obstructive andcentralapneas(combinedgroup)wereprospectivelyenrolledinthiscrosssectionalanalyticstudy.Allpatientsunderwentafullnight-attendedandafullnightCPAPtitrationpolysomnography.TitrationwasconsideredsuccessfulifAHI 10andthetitrationstudyincludedatleast15 min inREMstage. Results:OnCPAPtitration,thecombinedgroupshowedsignificantimprovementinsleepandrespiratorypolysomnographicparameters.MeanAHIwasreducedfrom71.9±30.3to 8.39±5.15(P=0.000).WhereasCPAPsignificantlyreducedthecentralapneaindexfrom 12.8±6.67to3.1±2.86(P=0.000),theresponsetocentraleventswasvariable(rangedfrom20%to100%).Overallresults,25(67.6%)hadsuccessfultitrationwithsignificantbetterresponseinfemalesthanmalestoCPAPthanmales(88.9%vs.60.7%,P=0.019). Conclusion:CPAPcanbeeffectiveincombinedobstructiveandcentralapneapatientswithoutheartfailurewithconsiderationofindividualvariability.AtrialofCPAPtitrationshouldbedoneinthosepatients. 2016TheEgyptianSocietyof ChestDiseasesandTuberculosis.Productionandhostingby ElsevierB.V.Thisisanopenaccessarticle under theCCBY-NC-ND license (http://creativecommons.org/licenses/by-nc-

AbstractContinuouspositiveairwaypressure(CPAP)isastandardtreatmentofmoderateandsevereobstructive sleepapnea syndrome.However, itseffect inpatients with coexistingobstructiveandcentralapneasiscontroversial. Objectives:TodeterminetheimmediateresponsetoCPAPincombinedobstructiveandcentralsleepapneapatientswithoutheartfailure. Methods:Thirty sevenconsecutivepatients with moderateandsevere coexisting obstructive andcentralapneas(combinedgroup)wereprospectivelyenrolledinthiscrosssectionalanalyticstudy.Allpatientsunderwentafullnight-attendedandafullnightCPAPtitrationpolysomnography.TitrationwasconsideredsuccessfulifAHI 10andthetitrationstudyincludedatleast15 min inREMstage. Results:OnCPAPtitration,thecombinedgroupshowedsignificantimprovementinsleepandrespiratorypolysomnographicparameters.MeanAHIwasreducedfrom71.9±30.3to 8.39±5.15(P=0.000).WhereasCPAPsignificantlyreducedthecentralapneaindexfrom 12.8±6.67to3.1±2.86(P=0.000),theresponsetocentraleventswasvariable(rangedfrom20%to100%).Overallresults,25(67.6%)hadsuccessfultitrationwithsignificantbetterresponseinfemalesthanmalestoCPAPthanmales(88.9%vs.60.7%,P=0.019). Conclusion:CPAPcanbeeffectiveincombinedobstructiveandcentralapneapatientswithoutheartfailurewithconsiderationofindividualvariability.AtrialofCPAPtitrationshouldbedoneinthosepatients. 2016TheEgyptianSocietyof ChestDiseasesandTuberculosis.Productionandhostingby ElsevierB.V.Thisisanopenaccessarticle under theCCBY-NC-ND license (http://creativecommons.org/licenses/by-nc-

Theimmunomodulatory effectsofantibioticscouldinfluencethedegreeofsystemicandlocalresponsestoinfection,soinvestigationoftheirintrinsicinfluenceonthehost’sinflammatoryresponseappearstobeessential.Fluoroquinolonesareknowntoexertmodulatoryactivityonimmuneresponsestomicrobialinfection.Howeverthemechanismofthisimmunmodulationhasnotbeenwellelucidated.Theaimofthework,istoassesstheimmunomodulatoryeffectsofalevofloxacin,throughexaminingitseffectontheconcentrationsoftumornecrosisfactorα(TNF-α)andInterleukin–10(IL-10)inserumofpneumonicpatients.Afterfollowinglocalresearchethicscommitteeapprovalandinformedconsent.Thisstudyincluded 40patientswithdifferenttypesofpneumonia,admittedtodepartmentofChestDiseases,FacultyofMedicine,AssiutUniversityHospitals,Egypt.Also,10healthyvolunteersservedasrandomizedcontrols.Bothpatientsandcontrolsreceivedlevofloxacin(750mgoncedailyfor10days).SerumlevelsofTNF-αandIL-10weremeasuredinpatientsandcontrolbeforeandafterlevofloxacinadministration(750mgoncedailyfor10days)usinghumanTNF–αandIL-10ELISAkitsrespectively.LevofloxacincausedastatisticallysignificantdecreaseinthemeanlevelofTNF-αinbothpatients(20.82±1.31pg/ml)(P0.009)andcontrolgroup(17.12±0.84pg/ml)(P0.004).Incontrast,therewasstatisticallysignificantincrease(P0.000)inthemeanlevelofIL-10inpatients (61.75±2.85pg/ml)whilestatisticallysignificantdecrease(P0.005)incontrolgroup(28.57±1.37pg/ml).Inconclusion,ourstudydemonstratesthattreatmentwithlevofloxacinaffectsproductionofTNF-αasapro-inflammatorycytokineandIL-10asananti-inflammatorycytokineswhichmayprovide additionalbenefitsintreatmentof respiratorytract infectionsthatare independentofitsantibacterialproperties.

Theimmunomodulatory effectsofantibioticscouldinfluencethedegreeofsystemicandlocalresponsestoinfection,soinvestigationoftheirintrinsicinfluenceonthehost’sinflammatoryresponseappearstobeessential.Fluoroquinolonesareknowntoexertmodulatoryactivityonimmuneresponsestomicrobialinfection.Howeverthemechanismofthisimmunmodulationhasnotbeenwellelucidated.Theaimofthework,istoassesstheimmunomodulatoryeffectsofalevofloxacin,throughexaminingitseffectontheconcentrationsoftumornecrosisfactorα(TNF-α)andInterleukin–10(IL-10)inserumofpneumonicpatients.Afterfollowinglocalresearchethicscommitteeapprovalandinformedconsent.Thisstudyincluded 40patientswithdifferenttypesofpneumonia,admittedtodepartmentofChestDiseases,FacultyofMedicine,AssiutUniversityHospitals,Egypt.Also,10healthyvolunteersservedasrandomizedcontrols.Bothpatientsandcontrolsreceivedlevofloxacin(750mgoncedailyfor10days).SerumlevelsofTNF-αandIL-10weremeasuredinpatientsandcontrolbeforeandafterlevofloxacinadministration(750mgoncedailyfor10days)usinghumanTNF–αandIL-10ELISAkitsrespectively.LevofloxacincausedastatisticallysignificantdecreaseinthemeanlevelofTNF-αinbothpatients(20.82±1.31pg/ml)(P0.009)andcontrolgroup(17.12±0.84pg/ml)(P0.004).Incontrast,therewasstatisticallysignificantincrease(P0.000)inthemeanlevelofIL-10inpatients (61.75±2.85pg/ml)whilestatisticallysignificantdecrease(P0.005)incontrolgroup(28.57±1.37pg/ml).Inconclusion,ourstudydemonstratesthattreatmentwithlevofloxacinaffectsproductionofTNF-αasapro-inflammatorycytokineandIL-10asananti-inflammatorycytokineswhichmayprovide additionalbenefitsintreatmentof respiratorytract infectionsthatare independentofitsantibacterialproperties.

Theimmunomodulatory effectsofantibioticscouldinfluencethedegreeofsystemicandlocalresponsestoinfection,soinvestigationoftheirintrinsicinfluenceonthehost’sinflammatoryresponseappearstobeessential.Fluoroquinolonesareknowntoexertmodulatoryactivityonimmuneresponsestomicrobialinfection.Howeverthemechanismofthisimmunmodulationhasnotbeenwellelucidated.Theaimofthework,istoassesstheimmunomodulatoryeffectsofalevofloxacin,throughexaminingitseffectontheconcentrationsoftumornecrosisfactorα(TNF-α)andInterleukin–10(IL-10)inserumofpneumonicpatients.Afterfollowinglocalresearchethicscommitteeapprovalandinformedconsent.Thisstudyincluded 40patientswithdifferenttypesofpneumonia,admittedtodepartmentofChestDiseases,FacultyofMedicine,AssiutUniversityHospitals,Egypt.Also,10healthyvolunteersservedasrandomizedcontrols.Bothpatientsandcontrolsreceivedlevofloxacin(750mgoncedailyfor10days).SerumlevelsofTNF-αandIL-10weremeasuredinpatientsandcontrolbeforeandafterlevofloxacinadministration(750mgoncedailyfor10days)usinghumanTNF–αandIL-10ELISAkitsrespectively.LevofloxacincausedastatisticallysignificantdecreaseinthemeanlevelofTNF-αinbothpatients(20.82±1.31pg/ml)(P0.009)andcontrolgroup(17.12±0.84pg/ml)(P0.004).Incontrast,therewasstatisticallysignificantincrease(P0.000)inthemeanlevelofIL-10inpatients (61.75±2.85pg/ml)whilestatisticallysignificantdecrease(P0.005)incontrolgroup(28.57±1.37pg/ml).Inconclusion,ourstudydemonstratesthattreatmentwithlevofloxacinaffectsproductionofTNF-αasapro-inflammatorycytokineandIL-10asananti-inflammatorycytokineswhichmayprovide additionalbenefitsintreatmentof respiratorytract infectionsthatare independentofitsantibacterialproperties.

Theimmunomodulatory effectsofantibioticscouldinfluencethedegreeofsystemicandlocalresponsestoinfection,soinvestigationoftheirintrinsicinfluenceonthehost’sinflammatoryresponseappearstobeessential.Fluoroquinolonesareknowntoexertmodulatoryactivityonimmuneresponsestomicrobialinfection.Howeverthemechanismofthisimmunmodulationhasnotbeenwellelucidated.Theaimofthework,istoassesstheimmunomodulatoryeffectsofalevofloxacin,throughexaminingitseffectontheconcentrationsoftumornecrosisfactorα(TNF-α)andInterleukin–10(IL-10)inserumofpneumonicpatients.Afterfollowinglocalresearchethicscommitteeapprovalandinformedconsent.Thisstudyincluded 40patientswithdifferenttypesofpneumonia,admittedtodepartmentofChestDiseases,FacultyofMedicine,AssiutUniversityHospitals,Egypt.Also,10healthyvolunteersservedasrandomizedcontrols.Bothpatientsandcontrolsreceivedlevofloxacin(750mgoncedailyfor10days).SerumlevelsofTNF-αandIL-10weremeasuredinpatientsandcontrolbeforeandafterlevofloxacinadministration(750mgoncedailyfor10days)usinghumanTNF–αandIL-10ELISAkitsrespectively.LevofloxacincausedastatisticallysignificantdecreaseinthemeanlevelofTNF-αinbothpatients(20.82±1.31pg/ml)(P0.009)andcontrolgroup(17.12±0.84pg/ml)(P0.004).Incontrast,therewasstatisticallysignificantincrease(P0.000)inthemeanlevelofIL-10inpatients (61.75±2.85pg/ml)whilestatisticallysignificantdecrease(P0.005)incontrolgroup(28.57±1.37pg/ml).Inconclusion,ourstudydemonstratesthattreatmentwithlevofloxacinaffectsproductionofTNF-αasapro-inflammatorycytokineandIL-10asananti-inflammatorycytokineswhichmayprovide additionalbenefitsintreatmentof respiratorytract infectionsthatare independentofitsantibacterialproperties.

ABSTRACT Community-acquiredpneumoniaisacommondiseaseandafrequentcauseofmorbidityandmortalityworldwide.HaemophilusinfluenzaeisaleadingcauseofCAP.ThecurrentstudywasconductedtodeterminetheserotypedistributionandantimicrobialsusceptibilitypatternsofHaemophilusinfluenzaeisolatedfromunvaccinatedadultpatientswithCAPatAssiutUniversityHospitals.MaterialsandMethods:FromSeptember2013toaugust2014,sputumsamplesfrom132adultpatientswithCAPwereanalyzedforthedetectionofHaemophilusinfluenzausingconventionalmethods.AntimicrobialsusceptibilityandserotypingofHaemophilusinfluenzaewasperformed.Results:Haemophilusinfluenzaeweredetectedin21(16%)CAP-patients.Non-typeableHinfluenzaewerethemostfrequentlyisolatedserotypethatfoundin15(71%)ofHinfluenzae-cases.Hinfluenzaetypebwasfoundin5(24%)cases.WhileHinfluenzaetypefwasfoundinone(5%)case.CasesweredetectedmainlyduringJanuary,February,andMarch.ResistancewashighestfortheB-lactamgroupofantibiotics.Conclusion:CAPhasadiseaseburdeninadultpatientsatAssiutUniversityHospitals,Egypt.HinfluenzaeisaleadingcauseofCAPwhichwasassociatedmostlywithnon-typeableserotypes.ResistancetopenicillinandotherantimicrobialagentsincreasedrapidlyduringthelastyearsamongH influenzaestrains. Keywords:Haemophilusinfluenzae,community-acquiredpneumonia,serotyping, antimicrobialresistance.

ABSTRACT Community-acquiredpneumoniaisacommondiseaseandafrequentcauseofmorbidityandmortalityworldwide.HaemophilusinfluenzaeisaleadingcauseofCAP.ThecurrentstudywasconductedtodeterminetheserotypedistributionandantimicrobialsusceptibilitypatternsofHaemophilusinfluenzaeisolatedfromunvaccinatedadultpatientswithCAPatAssiutUniversityHospitals.MaterialsandMethods:FromSeptember2013toaugust2014,sputumsamplesfrom132adultpatientswithCAPwereanalyzedforthedetectionofHaemophilusinfluenzausingconventionalmethods.AntimicrobialsusceptibilityandserotypingofHaemophilusinfluenzaewasperformed.Results:Haemophilusinfluenzaeweredetectedin21(16%)CAP-patients.Non-typeableHinfluenzaewerethemostfrequentlyisolatedserotypethatfoundin15(71%)ofHinfluenzae-cases.Hinfluenzaetypebwasfoundin5(24%)cases.WhileHinfluenzaetypefwasfoundinone(5%)case.CasesweredetectedmainlyduringJanuary,February,andMarch.ResistancewashighestfortheB-lactamgroupofantibiotics.Conclusion:CAPhasadiseaseburdeninadultpatientsatAssiutUniversityHospitals,Egypt.HinfluenzaeisaleadingcauseofCAPwhichwasassociatedmostlywithnon-typeableserotypes.ResistancetopenicillinandotherantimicrobialagentsincreasedrapidlyduringthelastyearsamongH influenzaestrains. Keywords:Haemophilusinfluenzae,community-acquiredpneumonia,serotyping, antimicrobialresistance.