Myocardial infarction (MI) is considered as the major cause of death and disability worldwide, and despite considerable advances in diagnosis and treatment, continues to be a major public health problem. Interleukin-17 (IL-17) is leukocyte-derived cytokine with effects especially on epithelial cells in various tissues. This study designed to investigate the level of IL-17 and its effect on lipid profile in patients with Acute Myocardial Infarction. The study included 50 patients with acute myocardial infarction forty healthy subjects as control group. The levels of IL-17 were significantly elevated in all patients groups (p < 0.001), total cholesterol, LDL, VLDL were significantly elevated (p < 0.001) in all patients as well.  There was positive correlation between IL-17 with HDL, while there was negative correlation with total cholesterol and LDL. The results show significant increase in levels of IL-17, in acute myocardial infarction patients. IL-17 positively correlated with HDL and negatively correlated with total cholesterol and LDL, which lead to consider it as cardio protective factor

Hasan, Hiba Ali

Ibrahim, Ammal Esmaeel

Jawad, Alaa Hussein

English

Myocardial infarction (MI) is considered as the major cause of death and disability worldwide, and despite considerable advances in diagnosis and treatment, continues to be a major public health problem. Interleukin-17 (IL-17) is leukocyte-derived cytokine with effects especially on epithelial cells in various tissues. This study designed to investigate the level of IL-17 and its effect on lipid profile in patients with Acute Myocardial Infarction. The study included 50 patients with acute myocardial infarction forty healthy subjects as control group. The levels of IL-17 were significantly elevated in all patients groups (p &lt; 0.001), total cholesterol, LDL, VLDL were significantly elevated (p &lt; 0.001) in all patients as well.  There was positive correlation between IL-17 with HDL, while there was negative correlation with total cholesterol and LDL. The results show significant increase in levels of IL-17, in acute myocardial infarction patients. IL-17 positively correlated with HDL and negatively correlated with total cholesterol and LDL, which lead to consider it as cardio protective factor

European Journal of Chemistry

European	Journal	of	Chemistry	5	(1)	(2014)	186‐188		European	Journal	of	Chemistry	ISSN	2153‐2249	(Print)	/	ISSN	2153‐2257	(Online)		2014	Eurjchem	Publishing	‐	Printed	in	the	USA	http://dx.doi.org/10.5155/eurjchem.5.1.186‐188.938					European	Journal	of	Chemistry	Journal	homepage:	www.eurjchem.com		 	 	IL‐17	level	in	patients	with	acute	myocardial	infarction	and		its	effect	on	lipid	profile	Ammal	Esmaeel	Ibrahim	a,*,	Hiba	Ali	Hasan	b	and	Alaa	Hussein	Jawad	a	a	Department	of	Chemistry,	College	of	Science,	Al‐Nahrain	University,	Baghdad,	10072,	Iraq	b	Department	of	Clinical	Laboratory	Science,	Collage	of	Pharmacy,	Al‐Mustansiriya	University,	Baghdad,	10052,	Iraq	*Corresponding	author	at:	Department	of	Chemistry,	College	of	Science,	Al‐Nahrain	University,	Baghdad,	10072,	Iraq.		Tel.:	+964.0790.1566784.	Fax:	+964.0790.1566784.	E‐mail	address:	dr.ammalalobaidi@yahoo.com	(A.E.	Ibrahim).				 		 	 	ARTICLE	INFORMATION	 	 ABSTRACT		DOI:	10.5155/eurjchem.5.1.186‐188.938	Received:	27	September	2013	Received	in	revised	form:	26	October	2013	Accepted:	26	October	2013	Online:	31	March	2014	KEYWORDS		 Myocardial	infarction	(MI)	is	considered	as	the	major	cause	of	death	and	disability	worldwide,and	despite	considerable	advances	in	diagnosis	and	treatment,	continues	to	be	a	major	publichealth	problem.	Interleukin‐17	(IL‐17)	is	leukocyte‐derived	cytokine	with	effects	especially	onepithelial	cells	in	various	tissues.	This	study	designed	to	investigate	the	level	of	IL‐17	and	itseffect	 on	 lipid	 profile	 in	 patients	 with	 Acute	 Myocardial	 Infarction.	 The	 study	 included	 50patients	with	acute	myocardial	infarction	forty	healthy	subjects	as	control	group.	The	levels	ofIL‐17	 were	 significantly	 elevated	 in	 all	 patients	 groups	 (p	 <	 0.001),	 total	 cholesterol,	 LDL,VLDL	 were	 significantly	 elevated	 (p	 <	 0.001)	 in	 all	 patients	 as	 well.	 	 There	 was	 positivecorrelation	 between	 IL‐17	 with	 HDL,	 while	 there	 was	 negative	 correlation	 with	 totalcholesterol	 and	 LDL.	 The	 results	 show	 significant	 increase	 in	 levels	 of	 IL‐17,	 in	 acutemyocardial	infarction	patients.	IL‐17	positively	correlated	with	HDL	and	negatively	correlatedwith	total	cholesterol	and	LDL,	which	lead	to	consider	it	as	cardio	protective	factor.	IL‐17	Triglycerides	Total	cholesterol	Low	density	lipoprotein	High	density	lipoprotein	Acute	myocardial	infarction		1.	Introduction		Interleukin‐17	is	a	member	of	polypeptides	family	with	six	different	 homodimeric	 cytokines	 (IL‐17A‐F)	 and	 the	 hetero‐dimeric	IL‐17A/F.	 Their	 interactions	with	 IL‐17	 receptors	A‐E	(IL‐17RA‐E)	mediate	 host	 defenses	while	 also	 contributing	 to	inflammatory	 and	 autoimmune	 responses.	IL‐17A	 and	IL‐17F	both	 preferentially	 engage	 a	 receptor	 complex	 containing	one	 molecule	 of	IL‐17RA	and	 one	 molecule	 of	IL‐17RC.	 More	generally,	IL‐17RA	appears	 to	 be	 a	 shared	 receptor	 that	 pairs	with	other	members	of	its	family	to	allow	signaling	of	different	IL‐17	 cytokines.	 Binding	 to	IL‐17RA	at	 one	 side	 of	 the	IL‐17A	molecule	 induces	 a	 conformational	 change	 in	 the	 second,	symmetry‐related	 receptor	 site	 of	IL‐17A.	 This	 change	 favors,	and	 is	 sufficient	 to	 account	 for,	 the	 selection	 of	 a	 different	receptor	 polypeptide	 to	 complete	 the	 cytokine‐receptor	complex.	 The	 structural	 results	 are	 supported	 by	 biophysical	studies	 with	IL‐17A	variants	 produced	 by	 site‐directed	mutagenesis	[1].	A	 unique	 intracellular	 signaling	 domain	 was	 identified	within	 all	 IL‐17Rs,	 termed	 similar	 expression	 to	 fibroblast	growth	factor	genes	and	IL‐17R	(SEFIR).	SEFIR	is	also	found	in	NF‐κB	activator	1.	However,	the	ligand	specificities	of	many	of	these	receptors	have	not	been	established.	The	IL‐17	signaling	system	 is	 operative	 in	 disparate	 tissues	 such	 as	 articular	cartilage,	 bone,	meniscus,	 brain,	 hematopoietic	 tissue,	 kidney,	lung,	 skin	 and	 intestine.	 Thus,	 the	 evolving	 IL‐17	 family	 of	ligands	 and	 receptors	 may	 play	 an	 important	 role	 in	 the	homeostasis	 of	 tissues	 in	 health	 and	 disease	 beyond	 the	immune	 system.	 This	 survey	 reviews	 the	biological	 actions	 of	IL‐17	signaling	in	cancers,	musculoskeletal	tissues,	the	immune	system	and	other	tissues	[2].	Interleukin	17	is	cytokine	which	acts	as	a	potent	mediator	in	delayed‐type	reactions	by	 increasing	chemokine	production	in	various	tissues	 to	recruit	monocytes	and	neutrophils	 to	 the	site	 of	 inflammation,	 similar	 to	 Interferon	 gamma.	 IL‐17	 is	produced	 by	 T‐helper	 cells	 and	 is	 induced	 by	 IL‐23	 which	results	 in	destructive	 tissue	damage	 in	delayed‐type	 reactions	[3].	 Interleukin	17	as	a	 family	 functions	as	a	proinflammatory	cytokine	 that	 responds	 to	 the	 invasion	of	 the	 immune	 system	by	 extracellular	 pathogens	 and	 induces	 destruction	 of	 the	pathogen’s	 cellular	 matrix.	 Interleukin	 17	 acts	 synergistically	with	tumor	necrosis	factor	and	interleukin‐1	[4].	Atherosclerosis	 is	 a	 lipid‐driven,	 chronic	 inflammatory	disease	 of	 the	 vessel	 wall	 in	 which	 both	 innate	 and	 adaptive	immune	 responses	 play	 a	 role	 [5].	 Immune	 cells	 and	 their	mediators	directly	cause	the	chronic	arterial	inflammation	that	is	 a	 hallmark	 of	 atherosclerosis.	Macrophages,	 T	 lymphocytes	and	 mast	 cells	 contribute	 to	 the	 smoldering	 inflammatory	response	in	the	vessel	wall	[6].		Ibrahim	et	al.	/	European	Journal	of	Chemistry	5	(1)	(2014)	186‐188	 187	 	Table	1.	Comparison	between	groups	for	Age,	BMI,	IL‐17,	and	lipid	profile.		Parameters		 AMI Control	Age	 63.0±8.7 60.00±6.36	BMI	 28.22±2.31 27.67±3.04	IL‐17	pg/mL 8.86±3.70 3.50±1.01	Total	cholesterol	 200.34±22.50 157.98±9.16 LDL	 186.9±25.4	 177.87±15.11	Triglyceride	 175.38±11.03	 155.53±24.09 VLDL	 35.13±19.22 31.14±12.10 HDL	 36.08±5.41 49.11±5.32 LDL/HDL		 5.16	 3.61	Total	cholesterol/	HDL	 5.55 3.30		The	 array	 of	 cytokines	 implicated	 in	 atherosclerosis	 is	strikingly	similar	to	those	used	by	immune	effector	cells	to	kill	foreign	 pathogens	 and	 defective	 or	 diseased	 host	 cells	 [7].	Virtually	every	major	cell	lineage	used	in	host	defense	has	been	identified	in	human	and/or	animal	plaques	[8].	This	study	designed	to	investigate	the	level	of	IL‐17	and	its	effect	 on	 lipid	 profile	 in	 patients	 with	 Acute	 Myocardial	Infarction.		2.	Experimental			This	 study	 was	 performed	 during	 the	 period	 from	December	2011	to	April	2012.	This	study	include	fifty	patients	with	 Acute	 Myocardial	 Infarction	 (AMI)	 were	 admitted	 to	Cardiac	Care	Unit	(CCU)	at	Medical	City	Teaching	Hospital	and	Ibn‐ALbetar	 Hospital	 in	 Baghdad	 patients,	 with	 rang	 50‐78	years	 old,	 were	 included	 in	 this	 study.	 Blood	 samples	 were	taken	from	the	patients	after	having	thoroughly	examined	after	exclusion	of	subjects	with	a	history	an	AMI	or	diabetes	mellitus	or	any	chronic	diseases.	Control	groups	 contain	 forty	 subjects	matched	 in:	 age,	 sex	 and	 BMI,	were	 included	 in	 this	 study	 as	control	group	(Table	1).		2.1.	Blood	collection	and	laboratory	analysis		From	 each	 patient	 and	 control,	 5	 mL	 venous	 blood	 was	aspirated	from	a	suitable	vein.	Samples	were	collected	between	8‐9	A.M.	after	10	hours	fast.	Blood	samples	were	transferred	to	plain	 tubes	 for	 storage	 to	measure	 IL17.	The	non‐heparinized	blood	in	the	plain	tubes	were	left	to	clot	and	than	centrifuged	at	4000	rpm	for	5	minutes	to	separate	the	serum	to	measure	the	lipid	 profile	 the	 remain	 of	 serum	 is	 dispensed	 into	 tightly	closed	 Eppendorf	 tubes	 in	 1.0	 mL	 and	 stored	 at	 ‐20	 °C	 until	assayed.	 Each	 serum	 sample	 was	 analyzed	 for	 urea	 and	creatinin	to	excluded	kidney	diseases.	IL‐17	measured	by	using	ELISA	kits	from	United	States	Biological	Company.		2.2.	Statistical	analysis		Statistical	analysis	was	performed	by	statisticians	with	the	SPSS	15.01	Statistical	Package	for	Social	Sciences	and	also	Excel	2003.	Data	 analysis	was	 done	 using	 chi‐square	 test	 for	 tables	with	frequencies,	while	we	used	independent	sample	t‐test	for	tables	with	means	 and	 standard	 deviations.	p	 value	 of	 ≤	 0.05	was	 used	 as	 the	 level	 of	 significance.	 Correlation	 coefficient	used	to	find	the	correlation	between	studied	markers	by	using	Pearson	 correlation.	 Descriptive	 statistics	 for	 the	 clinical	 and	laboratory	 results	 were	 formulated	 as	 mean	 and	 standard	error.		3.	Results	and	discussion			The	role	of	IL‐17A	to	atherogenesis	remains	controversial,	with	different	studies	proposing	either	a	pro‐atherogenic	or	an	athero‐protective	 contribution	 for	 IL‐17A.	 In	 patients	 with	unstable	angina,	 levels	of	plasma	IL‐17A	and	the	Th17‐related	cytokines	IL‐6	and	IL‐23	are	elevated	[9].		Emily	 Smith	 study	mention	 that	 ''the	 soluble	 levels	 of	 IL‐17A	 are	 elevated	 in	 the	 onset	 of	 acute	 coronary	 syndrome	compared	to	stable	angina	and	in	a	subset	of	aged	patients	with	coronary	 atherosclerosis	 and	 referent	 outpatients''	 [10].	Monocytes	 express	 IL‐17RA	 on	 their	 surface,	 and	 recent	 data	suggests	 that	 IL‐17A	 can	 also	 directly	 affect	 monocyte	chemotaxis	 in	 vivo	 and	 in	 vitro	 [11].	 There	 is	more	 than	 one	pathway	 by	 which	 IL‐17A	 might	 influence	 in	 local	inflammation.	IL‐17A	enhance	the	production	of	cytokines	and	chemokines	 in	 several	 cell	 types,	 including	 endothelial	 and	vascular	 smooth	muscle	 cells	 (VSMCs)	 [12],	 also	 IL‐17A	with	increase	 in	 IL‐2,	 IL‐6,	and	TNF‐α.	Study	by	Mohsen	Ibrahim	et	al.	 suggested	 that	 IL‐6	 is	 a	 pro‐atherogenic	 cytokine	 [13].	Increased	 in	 IL‐6	 was	 also	 associated	 with	 reduced	 collagen	content	 in	the	plaques,	blunted	synthesis,	and	release	of	 IL‐10	and	 diminished	 recruitment	 of	 inflammatory	 cells	 into	 the	atherosclerotic	 plaque.	 Elevated	 levels	 of	 IL‐6	 are	 also	 a	primary	stimulant	of	soluble	intercellular	adhesion	molecule‐1	(sICAM‐1),	 which	 mediates	 the	 attachment	 and	 migration	 of	leukocytes	 across	 the	 endothelial	 surface	 [13]	 soIL‐17A	 can	effect	on	plaques	by	indirect	way	by	increase	the	release	of	IL‐6.	 IL‐17A	also	synergistically	 initiate	production	of	CXCL1	and	CXCL10	 in	 cultured	 VSMCs	 [12].	 CXCL1	 is	 a	 chemokine	 that	causes	monocyte	capture	on	endothelium	during	atherogenesis	and	 therefore,	 acting	 a	 critical	 role	 in	 monocyte	 recruitment	into	artery	wall	[14].		Emily	 Smith,	 report	 that	 blocking	 IL‐17A	 in	 vivo	 lead	 to	reduced	CXCL1	expression	within	atherosclerosis‐prone	aortas	and	 weakened	 aortic	 macrophage	 content.	 Emily	 Smith	 also	prove	 that	 the	 pro‐inflammatory	 role	 of	 IL‐17A	 in	 the	regulation	 of	 monocyte	 migration	 into	 the	 aortas	 via	 ex	 vivo	monocyte	adhesion	assay,	thatpoint	toIL‐17A	contributes	in	the	pathogenesis	 of	 atherosclerosis	 through	 the	 controlling	 of	monocyte	enrollment	 to	 the	aortic	wall	 at	 least	via	CXCL1.	 IL‐17A	regulates	the	levels	of	G‐CSF	in	circulation	and	thus,	affects	neutrophil	 numbers	 in	 the	 blood.	 Cultured	 human	 T	 cells	isolated	from	atherosclerotic	coronary	arteries	also	produce	of	IL‐17A	 after	 polyclonal	 stimulation	 compared	 to	 T	 cells	extracted	from	non‐diseased	vessels	[10].	Administration	 of	 a	 rat‐anti‐mouse	 IL‐17A	 antibody	 into	Apoe‐/‐	 mice	 fed	 resulted	 in	 a	 50%	 reduction	 in	 aortic	 root	lesions.	 IL‐17A	 powerfullystimulates	 IL‐8	 and	 Vcam1	expression	 in	human	umbilical	vein	endothelial	 cells	 (HUVEC)	and	 apoptosis	 in	 vascular	 smooth	muscle	 cells	 (vSMCs),	 [15].	Gao	 et	 al.,	 examined	 the	 influence	 of	 rat‐anti‐mouse	 IL‐17A	neutralizing	 or	 isotype	 control	 Abs	 on	 rapid	 carotid	 stenosis	and	 atherosclerosis	 in	 Apoe‐/‐mice.	 Anti‐IL‐17A‐treated	 mice	showedaobviousreduces	in	aortic	root	plaque	size,	and	carotid	artery	 stenosis,	 and	 thatagreed	 with	 a	 decrease	 in	immunohistochemical	 MoMA2	 and	 α‐smooth	 muscle	 actin	staining	within	carotid	arteries	 [16].	Thus	suggest	 that	 IL‐17A	plays	 a	 pro‐inflammatory	 role	 in	 atherosclerosis	 through	 the	induction	of	aortic	chemokines,	cytokines,	and	accumulation	of	macrophages	within	atherosclerotic	plaques.	In	 the	 intact	 heart	 in	 vivo,	 IL‐17	 neutralization	 results	 in	reduced	necrotic	and	apoptotic	myocyte	death,	suggesting	that	inhibition	of	the	IL‐17	pathway	may	be	of	therapeutic	benefit	in	human	Myocardial	Infarction.	188	 Ibrahim	et	al.	/	European	Journal	of	Chemistry	5	(1)	(2014)	186‐188			Table	2.	The	correlation	(r)	between	IL‐17	with	(lipid	profile)	for	studied	group.			IL‐17	 involved	 in	 the	 clearance	 of	 extracellular	 pathogens	and	has	been	consider	as	a	driving	force	in	many	inflammatory	diseases	[17].	Our	 study	 contradict	 with	 the	 study	 that	 found	 patients	with	 higher	 IL‐17	 levels	 had	 reduced	 risk	 of	 major	cardiovascular,	in	this	study	risk	factors	are	the	cholesterol	and	LDL‐cholesterol,	 events	 may	 provide	 further	 evidence	 of	 a	beneficial	 role	of	 IL‐17.In	mice	with	myocardial	 infarction,	 IL‐17	may	be	used	therapeutically	for	treating	MI,	considering	that	it	may	ameliorate,	rather	than	exacerbate,	the	disease	[18].	The	 negative	 correlation	 between	 IL‐17	 A	 and	 total	cholesterol	as	well	as	LDL‐C	in	our	study	may	suggest	that	the	increased	level	of	IL‐17	stimulate	LDL‐C	receptor	expression	in	hepatic	cell	that	subsequently	 lead	to	increased	uptake	of	LDL	particles	and	decreased	LDL‐C	plasma	level	[19].	In	 Table	 2	 our	 results	 show	 that	 highly	 significant	negativecorrelation	 between	 IL‐17	 and	 all	 lipid	 profile	 except	for	 HDL	 which	 show	 highly	 significant	 positive	 correlation,	these	 findings	 suggest	 that	 increase	 in	 IL‐17	 level	 isaffect	myocardial	infarction	via	dyslipidemiaso	that	make	us	consider	it	 as	 cardiovascular	 protective	 factor.	 Proinflammatory	cytokines	are	known	to	contribute	to	features	of	the	metabolic	syndrome,	 such	 as:	 hypertension,	 dyslipidemia,	 insulin	resistance,	 endothelial	 dysfunction,	 clotting	 system	 activation,	pro‐oxidative	 stress	 and	 pathogenesis	 of	 atherosclerosis	[15,20].	HDL‐C	 has	 antioxidant	 and	 anti‐inflammatory	 properties	also	 have	 anticoagulant	 effect	 and	 enhances	 half‐life	 of	 post	stacyclin.	 The	 anti‐inflammatory	 properties	 of	 HDL‐C	may	 be	particularly	 relevant	 here,	 because	 we	 observed	 systematic	inflammation	 and	 endothelial	 activation	 in	 patients	 with	 low	HDL‐C	level	[21].	Our	result	of	positive	correlation	between	IL‐17	 and	 HDL	 is	 may	 be	 because	 several	 proinflammatory	cytokines	 have	 been	 implicated	 in	 the	 overall	 regulation	 of	plasma	HDL	concentrations	 [22].	This	 finding	 is	disagreement	with	 results	 from	 previous	 studies	 which	 reports	 that	 IL‐17	expression	 is	 up	 regulated	 under	 hypercholesterolemia	conditions	 [22‐24].	 Another	 study	 show	 that	 cholesterol	incubation	 significantly	 increases	 IL‐17A	production,	which	 is	consistent	 with	 findings	 in	 mice	 that	 a	 high‐fat	 diet	 leads	 to	increased	IL‐17A	production	[25].	Also,	IL‐17A	Ab‐treated	mice	have	 reduced	 atherosclerotic	 lesions	 in	 the	 presence	 of	unchanged	serum	cholesterol	and	HDL/LDL	ratio,	therefore	IL‐17A	 is	 unlikely	 to	 affect	 atherogenesis	 via	 changes	 in	hyperlipidemia	or	production	of	oxLDL	Abs	[15].		4.	Conclusion			The	 results	 show	significant	 increase	 in	 levels	 of	 IL‐17,	 in	acute	 myocardial	 infarction	 patients.	 IL‐17	 positively	correlated	 with	 HDL	 and	 negatively	 correlated	 with	 total	cholesterol	 and	 LDL,	 so	 that	 make	 us	 consider	 it	 as	 cardio	protective	factor.		References		[1]. Liu,	 S.;	 Song,	 X.;	 Chrunyk,	 B.	 A.;	 Shanker,	 S.;	 Hoth,	 L.	 R.;	 Marr,	 E.	 S.;	Griffor,	M.	C.	Nature	Commun.	2013,	4,	1888‐1888.	[2]. Zhang,	B.;	 Liu,	 C.;	Qian,	W.;	Han,	Y.;	 Li,	X.;	Deng,	 J.	 J.	 Immunol.	2013,	190(5),	2320‐2326.		[3]. Janis,	 K.;	 Thomas,	 J.;	 Richard,	 A.;	 Barbara,	 A.	 Kuby	 Immunology.	 San	Francisco,	W.	H.	Freeman,	2007,	pp.	396.	[4]. Chiricozzi,	 A.;	 Guttman‐Yassky,	 E.;	 Suarez‐Farinas,	M.;	 Nograles,	 KE.;	Tian,	 S.;	 Cardinale,	 I.;	 Chimenti,	 S.;	 Krueger,	 J.	 G.	 J.	 Invest.	Dermatol.	2011,	131(3),	677‐687.		[5]. Huang,	C.	S.;	Timothy,	R.;	Arditi,	M.	Innate	Immun.	2010,	2,	325‐333.		[6]. Hansson,	G.	K.;	Libby,	P.;	Schonbeck,	U.;	Yan,	Z.	Q.	Circ.	Res.	2002,	9(1),	281‐291.		[7]. Hansson,	G.	K.	N.	Engl.	J.	Med.	2005,	352(16),	1685‐1695.		[8]. O’Connor,	W.;	Kamanaka,	M.;	Booth,	C.	J.;	Town,	T.;	Nakae,	S.;	Iwakura,	Y.;	Kolls,	J.	K.;	Flavell,	R.	A.	Nat.	Immunol.	2009,	10,	603‐609.		[9]. Butcher,	M.;	Galkina,	E.	Thromb.	Haemost.	2011,	106,	787‐795.		[10]. Smith,	E.;	Konkal‐Matt,	R.;	Prasad,	M.	B.;	AncaDobrian,	J.	K.;	Kolls,	K.	L.;	Elena,	G.	Circulation	2010,	121(15),	1746‐1755.		[11]. Sergejeva,	 S.;	 Ivanov,	 S.;	 Lotvall,	 J.;	Linden	A.	 J.	Respir.	Cell.	Mol.	Biol.	2005,	33,	248‐253.		[12]. Rao,	D.	A.;	 Eid,	R.	E.;	Qin,	 L.;	 Yi,	 T.;	 Kirkiles‐Smith,	N.	C.;	Tellides,	G.;	Pober,	J.	S.	J.	Exp.	Med.	2008,	205,	3145‐3158.		[13]. Mohsen,	I.	M.	Obes.	Rev.	2010,	11,	11‐18.		[14]. Erbel,	C.;	Chen,	L.;	Bea,	F.;	Wangler,	S.;	Celik,	S.;	Lasitschka,	F.;	Wang,	Y.;	Bockler,	D.;	Katus,	H.	A.;	Dengler,	T.	J.	J.	Immunol.	2009,	183,	8167‐8175.		[15]. Taleb,	S.;	Tedgui,	A.;	Mallat,	Z.	Curr.	Opin.	Pharmacol.	2010,	10,	 197‐202.	[16]. Gao,	Q.;	 Jiang,	Y.;	Ma,	T.;	Zhu,	F.;	Gao,	F.;	Zhang,	P.;	Guo,	C.;	Wang,	Q.;	Wang,	X.;	Ma,	C.;	Zhang,	Y.;	Chen,	W.;	Zhang,	L.	J.	Immunol.	2010,	185,	5820‐5827.		[17]. Barry,	 S.	 P.;	 Ounzain,	 S.;	 Cormick,	 J.	 A.;	 Scarabelli,	 T.	 M.;	 Chen‐Scarabelli,	C.;	Saravolatz,	L.	 I.	 I.;	Faggian,	G.;	Mazzucco,	A.;	Suzuki,	H.;	Thiemermann,	 C.;	Knight,	 R.	A.;	 Latchman,	D.	 S.;	 Stephanou,	A.	 Int.	 J.	Cardiol.	2013,	163,	326‐334.		[18]. Troitskaya,	 M.;	 Baysa,	 A.;	 Vaage,	 J.;	 Sand,	 K.	 L.;	 Maghazachi,	 A.	 A.;	Valen,	G.	Toxins.	2012,	4,	1427‐1439.		[19]. Zuniga,	L.	A.;	Shen,	W.	J.;	Joyce‐Shaikh,	B.;	Pyatnova,	E.	A.;	Richards,	A.	G.;	 Thom,	 C.;	 Andrade,	 S.	 M.;	 Cua,	 D.	 J.;	 Fredric	 B.	 Kraemer,	 F.	 B.;	Butcher,	E.	C.	J.	Immunol.	2010,	185(11),	6947‐6959.		[20]. Nuzhatun,	N.;	Qazi,	M.	A.	Indian	J.	Dermatol.	Venereol.	Leprol.	2010,	76,	662‐665.		[21]. Gastro,	A.	Am.	J.	Resp.	Crit.	Care	2010,	182(5),	661‐668.		[22]. Canizales‐Quinteros,	 S.;	 Aguilar‐Salinas,	 C.	 A.;	 Reyes‐Rodriguez,	 E.;	Riba,	L.;	Rodriguez‐Torres,	M.;	Ramirez‐Jimenez,	S.;	Huertas‐Vazquez,	A.;	 Fragoso‐Ontiveros,	V.;	Zentella‐Dehesa,	A.;	Ventura‐Gallegos,	 J.	 L.;	Vega‐Hernandez,	 G.;	 Lopez‐Estrada,	 A.	 Auron‐Gomez,	 M.;	 Gomez‐Perez,	F.;	Rull,	 J.;	Cox,	N.	 J.;	Bell,	G.	 I.;	Maria	Teresa	Tusie‐Luna,	M.	T.	Circ.	Res.	2003,	92,	569‐576.		[23]. Al‐Aubaidy,	H.	A.;	Sahib,	H.	A.;	Mohammad,	B.	I.;	Hadi,	N.	R.;	Abas,	S.	M.	J.	Pharm.	Tech.	Drug	Res.	2013,	2,	11.	DOI:	10.	7243/2050‐120X‐2‐11.		[24]. Smith,	E.;	 Prasad,	K.	M.;	Butcher,	M.;	Dobrian,	A.;	Kolls,	 J.	K.;	 Ley,	K.;	Galkina,	E.	Circulation	2010,	121,	1746‐1755.		[25]. Brull,	 F.;	Mensink,	R.	 P.;	 Steinbusch,	M.	F.;	Husche,	C.;	 Lutjohann,	D.;	Wesseling,	G.;	Plat,	J.	PLOS	One.	2012,	7(10),	e46895.		p	value		r	Parameters	<0.001	‐0.453Total	cholesterol	<0.001	‐0.385	LDL	<0.001	‐0.246Triglyceride	<0.001	‐0.246	VLDL	<0.001	+0.351	HDL	

IL-17 level in patients with acute myocardial infarction and  its effect on lipid profile

Ammal Esmaeel Ibrahim

Hiba Ali Hasan

Alaa Hussein Jawad

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IL-17 level in patients with acute myocardial infarction and its effect on lipid profile

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IL-17 level in patients with acute myocardial infarction and its effect on lipid profile

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