









































  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

 
 

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. 

PULMONARY  
INFLAMMATION & INJURY 
IN A MOUSE MODEL OF 

NON-ALCOHOLIC  
STEATOHEPATITIS  

TANVI BANOTA, ALEXA MURRAY, LAURA E. ARMSTRONG,  
BO KONG, GRACE L. GUO, ANDREW J. GOW, 

DEBRA L. LASKIN (FACULTY ADVISOR) 

 
 

✵ ABSTRACT 
Non-alcoholic fatty liver disease (NAFLD) is a chronic 
liver condition that affects millions of individuals in 
the United States, of which approximately twenty 
percent of cases progress to non-alcoholic steato-
hepatitis (NASH). NASH is characterized by macro-
vascular steatosis and persistent inflammation in the 
liver, which can lead to fibrosis. Evidence suggests 
potential effects of NAFLD and NASH on the devel-
opment of pulmonary pathologies, but the interac-
tion between the liver and the lung is not well under-
stood. In this study, we assessed the impact of NASH 
development on lung inflammation and fibrosis over 
time. Male C57BL/6J mice were fed control (10% 
kCal) or high-fat (HFD) (60% kCal) diets. Liver tissue, 
lung tissue, and bronchoalveolar lavage (BAL) fluid 
were collected after 1, 3, and 6 months of feeding. 
Histopathologic evaluation of livers from HFD-fed 
mice at 6 months confirmed the development of 
NASH. In the lung, we observed histopathologic al-
terations, including inflammatory cell infiltration, li-
pid-laden macrophages, septal damage, and epi-
thelial thickening at 6 months. Gene expression anal-
ysis of whole lung tissue revealed changes in genes 
related to inflammation (IL-1B), fibrosis (CTGF), and 
lipid metabolism (ApoA1). These results characterize 
an association of pulmonary complications during 
simple steatosis to NASH transition, suggesting 
lung-liver crosstalk. 

1 INTRODUCTION 
Non-alcoholic fatty liver disease (NAFLD) is 

a chronic liver condition that is estimated to affect 
upwards of thirty percent of individuals in the United 
States, with even more at risk due to the rising obe-
sity epidemic.[3,5,19] NAFLD is characterized by the ac-
cumulation of fat in the liver, known as steatosis. It is 
estimated that twenty percent of patients diagnosed 
with NAFLD progress to non-alcoholic steatohepati-
tis (NASH).[21] NASH is a severe, chronic liver disease 
characterized by persistent inflammation and im-
mune cell infiltration. NASH may also progress to fi-
brosis and cirrhosis of the liver—this irreversible scar-
ring of tissue can further lead to uncontrolled cell 
growth, cancer, and death. NASH is becoming the 
leading indication for liver transplantation in both 
the U.S. and worldwide.[2,14,16] 

Both NAFLD and NASH are associated with 
systemic effects that manifest in pathologies across 
the body, including cardiovascular disease, meta-
bolic syndrome, and chronic kidney conditions.[1] 
Emerging evidence also suggests that NAFLD and 
NASH may impact the development of pathologies 
in the lung. Several longitudinal observational stud-
ies have detailed an association between NAFLD 
and decreased measurements of lung function (e.g. 
forced expiratory volume and vital capacity).[7,11,12,15] 
In addition, patients with chronic obstructive pulmo-
nary disease (COPD) showed increased incidence of 
both NAFLD and NASH.[20] Although there is rising 
clinical evidence of a relationship between NASH 
and reduced pulmonary function, the interplay be-
tween the liver and the lung remains largely unex-
plored.  

A central aspect of NAFLD and NASH that 
may contribute to lung injury is inflammation. Key 
players in this response are macrophages, phago-
cytic cells of the innate immune system. In the liver, 
macrophages are known to take up surrounding fat 
through endocytosis. This causes the macrophages 
to become activated and release pro-inflammatory 
mediators such as cytokines, small proteins im-
portant in inflammatory cell signaling.[14] These me-
diators enter the bloodstream and can exert effects 
in other tissues of the body through systemic circu- 



  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

lation, leading to observed comorbidities.[1,9,14] We 
hypothesize that these inflammatory mediators ac-
cumulate in the lung, causing pulmonary injury, in-
flammation, and the disruption of key signaling path-
ways by dysregulating genes related to lipid metab-
olism and inflammation, including Il-1B, Ctgf, Lxr, 
ApoA1, and Abca1. The present study was designed 
to test this hypothesis and characterize the develop-
ment of lung injury in a high fat diet mouse model of 
NASH. The results of our study provide data on lung-
liver crosstalk, which may be useful for the develop-
ment of new approaches for clinical management of 
pulmonary pathology related to NASH.  

 

2 METHODOLOGY  

ANIMALS & TREATMENTS 

Wild type male C57BL/6J mice (6-8 weeks,  
𝑛𝑛 = 5 − 9/group) were fed control (10% kCal) or a 
high-fat diet (HFD) (60% kCal) for 1, 3, and 6 months. 
Food consumption was monitored weekly. Animal 
protocols were approved by Rutgers University 
IACUC. 
 
HISTOLOGICAL ANALYSIS 

Liver and lung tissue were collected, fixed in 10% for-
malin or inflated and fixed in 4% paraformaldehyde, 
respectively, and cut into 5-μm sections and stained 
with hematoxylin & eosin (H&E). Lung sections were 
evaluated for characteristics of lung injury and in-
flammation, including inflammatory cell infiltration, 
septal damage, and epithelial thickening. Liver sec-
tions were examined for the histopathological char-
acteristics of NAFLD (e.g. fat accumulation) and 
NASH (e.g. fat accumulation and inflammatory cell 
infiltration) based on established criteria.[2,16] 
 
BRONCHOALVEOLAR LAVAGE (BAL) CELL AND PROTEIN  
MEASUREMENT 

BAL fluid was collected by 
slowly instilling and withdraw-
ing 1 mL of ice-cold (4°C) PBS 
into the lungs of mice through 
a cannula in the trachea  
(FIGURE 1). This fluid was centri-
fuged at 300xg for 8 minutes. 
Cell pellets were resuspended 

in 1 mL of PBS. Viable cells (10 μl) were counted on 
a hemocytometer using trypan blue dye exclusion. 
Cytospins were prepared by centrifugation of 104 

cells BAL fluid onto microscope slides using a Shan-
don cytospin (Thermo Scientific).  Cells were fixed in 
methanol and stained with Giemsa to visualize BAL 
cell populations. Total protein content in cell free 
BAL was quantified using a BCA protein kit (Pierce 
Biotechnologies Inc.) with bovine serum albumin as 
the standard. All samples were assayed in triplicate 
at 562 nm using a spectrophotometer.  
 
MRNA ISOLATION AND RT-QPCR ANALYSIS 

Total RNA was extracted from lung tissue using TRI-
zol Reagent and bead TissueLyser LT (Qiagen). 
cDNA was generated using High Capacity cDNA Re-
verse Transcription kit (Applied Biosystems). Real-
time quantitative PCR (RT-qPCR) was performed on 
a QuantStudio 6 system using commercially availa-
ble Power SYBR® Green gene expression assays 
(Applied Biosystems). Data were normalized to β-ac-
tin and presented as fold change relative to 1 month 
CTRL mice. Fold changes in gene expression were 
calculated using ∆∆𝐶𝐶𝐶𝐶 method where 
𝐶𝐶𝐶𝐶(𝐶𝐶𝑡𝑡𝑡𝑡𝑡𝑡𝑡𝑡𝐶𝐶 𝑡𝑡𝑡𝑡𝑛𝑛𝑡𝑡) –  𝐶𝐶𝐶𝐶(𝛽𝛽 − 𝑡𝑡𝑎𝑎𝐶𝐶)  =  ∆𝐶𝐶𝐶𝐶; 
∆𝐶𝐶𝐶𝐶 –  𝑡𝑡𝑎𝑎𝑡𝑡𝑡𝑡𝑡𝑡𝑡𝑡𝑡𝑡 ∆𝐶𝐶𝐶𝐶(1 𝑀𝑀𝑀𝑀𝑛𝑛𝐶𝐶ℎ 𝐶𝐶𝐶𝐶𝐶𝐶𝐶𝐶)  =  ∆∆𝐶𝐶𝐶𝐶; and 
2 − ∆∆𝐶𝐶𝐶𝐶 =  𝑓𝑓𝑀𝑀𝑓𝑓𝑓𝑓 𝑎𝑎ℎ𝑡𝑡𝑛𝑛𝑡𝑡𝑡𝑡. 
 

STATISTICAL ANALYSIS  

Data are presented as mean + SE and were analyzed 
using 2-way ANOVA and Sidak’s multiple compari-
sons test. A p-value ≤0.05 was considered statisti-
cally significant.  

 
3 RESULTS 
HIGH-FAT DIET INDUCES NASH AND CAUSES HISTOPATHOLOGICAL 

CHANGES IN THE LUNG 

To confirm the development of NASH, we assessed 
histopathological changes in the liver. Livers from 
mice fed a HFD for 1 and 3 months exhibited steato-
sis, or the accumulation of lipid droplets in the liver, 
but no inflammatory cell infiltration, indicating 
NAFLD (data not shown). The most prominent 
changes in the liver were observed 6 months follow-
ing consumption of a HFD; these included more se-
vere steatosis and infiltration of inflammatory cells 

 

FIGURE 1  



  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

(FIGURE 2A). Significant increases in body weights, in-
creases in total serum cholesterol, and decreased 
glucose tolerance in HFD-fed mice confirmed this 
was metabolic syndrome-related NASH (data not 
shown). We next assessed alterations in lung histol-
ogy. After 6 months, inflammatory cell infiltration, 
septal damage, and epithelial thickening were ob-
served in HFD-fed mice relative to mice fed the con- 

trol diet (FIGURE 2B). The accumulation of large macro- 
phages in the lung that appeared lipid-laden was 
also noted in the histology. Further examination of 
cell cytospins also revealed the presence of large, 
vacuolated, and potentially lipid-laden macro-
phages (FIGURE 2B inserts). We further investigated 
lung injury and inflammation by quantifying levels of 
BAL protein and cells, respectively (FIGURE 2C). Alt-  

FIGURE 2: Representative images of H&E stained sections of liver (PANEL A) and lung (PANEL B) from mice fed control (CTRL) or 
high fat diets (HFD) for 6 months. PANEL A, left arrow indicates steatosis, right arrow and inset indicates inflammation. PANEL B, 
top arrow indicates inflammatory cell infiltration and bottom arrow indicates epithelial thickening. PANEL B insets highlight rep-
resentative macrophages from Giemsa-stained cytopsins, including macrophages with a large, lipid-laden appearance in 
HFD-fed mice. Original magnification (A) 4x or (B) 20x, inserts 40x. (C) BAL collected from mice 1, 3, and 6 months after a 
control (CTRL) or high fat diet (HFD) was assessed for protein and cell content. Bars, mean + SE (n=5-10).  

*Significantly different from CTRL fed mice.  

#Significantly different from 1 month.  

aSignificantly different from 3 month.  
 



  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

hough increased lung injury was noted in HFD-fed 
mice at 6 months as measured by BAL protein, this 
may be due to a reduction in BAL protein in control 
mice at this time. Surprisingly, a time related in-
crease in lung inflammation was observed in control 
mice at 3 and 6 months. Cell counts were unaffected 
by administration of the HFD.  
 

HIGH FAT DIET DISRUPTS EXPRESSION OF INFLAMMATORY AND LIPID 

METABOLISM RELATED GENES 

To better understand degrees of inflammatory 
changes in the lung following a HFD, we analyzed 
expression of inflammatory and lipid-related genes. 
Expression of interleukin 1 beta (Il-1b), a key early re-
sponse proinflammatory gene, was significantly in-
creased in mice fed a HFD when compared to con- 

FIGURE 3: Lung tissue collected 1, 3, and 6 months after control (CTRL) or high fat diet (HFD) from mice were analyzed for gene 
expression by RT-qPCR. Data were normalized relative to ß-actin and presented as fold change relative to 1 Month CTRL fed 
mice. Bars, mean + SE (n=3-7).  

*Significantly different from CTRL fed mice.  

#Significantly different from 1 month.  

aSignificantly different from 3 month.  
 



  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

trol mice at 3 months. Il-1b expression returned to 
control levels by 6 months. The expression of con-
nective tissue growth factor (Ctgf), a gene indicative 
of fibrosis and tissue remodeling, was significantly 
decreased 1 month following HFD-feeding. Interest-
ingly, control mice displayed a significant decrease 
in Ctgf at 3 and 6 months when compared to 1 
month. Similarly, expression of apolipoprotein A1 
(Apoa1), a lipid chaperone, was decreased 1 month 
following HFD when compared to control-fed mice. 
ApoA1 expression was similarly reduced in the 6-
month control-fed mice when compared to 1-month 
control mice. There were no changes in expression 
of liver X receptor (Lxr), a nuclear receptor involved 
in lipid homeostasis, and its target ATP-binding cas-
sette transporter 1 (Abca1), a lipid transporter. 
 

4 DISCUSSION  
The inflammatory and fibrogenic effects of 

NASH in the liver have been well characterized.[2,14] 
Emerging clinical evidence suggests that NAFLD 
and NASH are associated with pulmonary injury, but 
crosstalk between the lung and the liver in NASH has 
not been investigated.[7,11,12,15] In these studies, we 
used a mouse model of HFD to induce NASH and 
investigate associated injury and inflammation in the 
lung. We found that NASH was associated with his-
topathological alterations in lung tissue 6 months 
post HFD feeding; moreover, expression of genes 
related to inflammation and lipid metabolism was 
dysregulated throughout NAFLD development, in-  
cluding the progression to NASH. These results pro-
vide insights into the interplay between liver and 
lung inflammation and highlight potential inflamma-
tory pathways for crosstalk between the tissues.  

Based on established criteria, we confirmed 
the development of NASH in mice fed a HFD as we 
observed increased steatosis and inflammatory cell 
infiltration at 6 months.[2,16] This was correlated with 
pulmonary histopathological changes in the HFD-
fed mice at this time. Further assessment by a 
pathologist will be completed to confirm these his-
topathological changes. Although there was no evi-
dence of pulmonary fibrosis in these animals, we 
noted the appearance of lipid-laden macrophages 
in the lung. These cells have been shown to be asso- 

ciated with fibrosis in other disease states, and may 
contribute to the development of lung fibrosis at 
later time points in NASH.[18] Interestingly, histo-
pathological changes in the lung were not reflected 
by increases in BAL protein or cell counts, which are 
markers of pulmonary alveolar epithelial damage 
and leaky vasculature, or infiltration of immune cells 
into the lung in response to injury.[17] It may be that 
NASH is not associated with epithelial barrier dys-
function and that pathologic alterations involve 
other mechanisms of injury. For example, it is possi-
ble that resident macrophages present in the lung 
are activated following HFD and that they drive lung 
inflammation. Further studies are needed to explore 
this possibility. We also noted a decrease in BAL pro-
tein content at 6 months and increases in BAL cells 
in control mice; this may be indicative of age-related 
changes in tissue structure or vasculature, or in basal 
inflammatory activity.[4] HFD-fed mice seem to also 
mimic this age-related trend of increasing inflamma-
tion, although not significantly. 

We speculated that histopathological 
changes in the lung of animals fed a HFD might be 
driven by differential expression of genes related to 
inflammatory proteins and cytokines. In this context, 
our gene expression analyses revealed increases in 
Il-1b at 3 months in HFD-fed mice, which suggests 
that during the development of NASH, the lung re-
sponds to hepatic inflammation by upregulating in-
flammatory gene expression. IL-1β is an early re-
sponse cytokine known to promote inflammation; 
thus, increases in inflammatory cells in the lung of 
mice fed a HFD may be mediated in part by this cy-
tokine. We also observed early downregulation of 
Apoa1 in HFD-fed mice at 1 month. ApoA1 is a lipid 
chaperone that promotes the efflux of cholesterol; it 
has been shown to have anti-inflammatory and anti-
fibrotic effects in the lung.[6,8] The observed decrease 
in ApoA1 may further exacerbate inflammation in 
the lung in response to a HFD. Although we did not 
observe lung fibrosis during the histopathological 
analysis, we assessed changes in CTGF gene expres-
sion as a measure of fibrotic extracellular matrix tis-
sue remodeling.[10,13] Ctgf expression was decreased 
in HFD-fed mice at 1 month, suggesting that a HFD 
may suppress fibrotic mechanisms in the lung early 



  ARESTY  RUTGERS UNDERGRADUATE RESEARCH JOURNAL, VOLUME I, ISSUE III 
 
 
 

in the process of NASH development. This might be 
a compensatory response to prevent fibrosis in-
duced by other growth factors generated in the lung 
in response to the HFD. A similar decrease in Ctgf 
expression at 3 and 6 months in the control mice in-
dicates that the HFD may be mimicking age-related 
effects in mice as early as 1 month.  

While these data provide preliminary char-
acterization of pulmonary changes in a mouse 
model of NASH, experiments to confirm the pres-
ence of lipid-laden macrophages by staining for li-
pids as well as an assessment of histopathological 
changes by a pathologist will be conducted. Future 
studies will also be performed to further elucidate 
mechanisms of high fat diet-associated effects on 
the lung, including assessment of systemic markers 
of lipid dysregulation, liver inflammation and dys-  
function, and other inflammatory signaling pathways 
in the lung. Developing our understanding of the in-
terplay between the lung and the liver can help iden-
tify the mechanisms by which disease can influence 
distant pathologies, and how inflammation in partic-
ular can be controlled to limit pathological comor-
bidities in patients.   

 

5 CONCLUSION 
Overall, these data demonstrate that HFD-

induced NASH leads to pulmonary histopathologi-
cal changes. Moreover, these changes may be 
driven by the dysregulation of key mediators in-
volved in inflammation and lipid metabolism. This 
analysis of lung-liver crosstalk in NASH highlights po-
tential for the clinical management of pulmonary 
complications associated with NASH∎  
 

6 ACKNOWLEDGEMENTS 
I would like to acknowledge everyone in Dr. Debra 
Laskin’s lab for their guidance and support, espe-
cially Dr. Alexa Murray and Dr. Debra Laskin. I would 
also like to acknowledge Dr. Bo Kong for his exper-
tise and guidance with the animals used in this pro-
ject, Dr. Laura Armstrong for providing liver images, 
and Dr. Grace Guo for her continued scientific guid-
ance. This research was supported by NIH Grants 
ES029258, ES005022, and ES004738. 

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Tanvi Banota is a senior in the Honors College at Rutgers University majoring in Cell Biology and 
Neuroscience and minoring in Linguistics. She has been conducting research in the Laskin Lab 
since high school when she was first matched with the lab through the Liberty Science Center Part-
ners in Science Program. Her research is on the mechanisms of inflammation following toxicant-
induced pulmonary injury. Tanvi plans to pursue an MD/PhD after Rutgers and hopes to have a 
career running her own lab, seeing patients, and mentoring students. Outside of academics and 
research, Tanvi is an epee fencer on the Rutgers Fencing Team, is highly involved with the Aresty 
Research Center, and enjoys watching sports, spending time with her friends, and playing and lis-
tening to music. Tanvi was also a part of the founding team for the Aresty RURJ in 2019 and has 
served as a peer reviewer, senior peer reviewer, and editor for the journal. She’s excited to see 
where the journal will go next and how it will continue to uplift and represent the undergraduate 
research community at Rutgers! For any questions, please contact Tanvi at: 
TANVI.BANOTA@RUTGERS.EDU 
 

 


